Since we have over 10,000 men on this forum and just a few of you reply to transdermal estradiol posts, I really am curious as to how many are using this 'novel' (for lack of a better word) form of ADT exclusively? I for one and a few comrades that I have befriended here are having 'damn' good luck with E2 (estradiol) patches, gels and cremes.
I imagine most of you know something about the old, synthetic, oral estrogen DES (diethylstilbestrol) that was used as ADT until the mid 80's when it was discontinued and replaced with Lupron (leuprolide). Despite the ~30% increase in CV events, DES was quite effective in keeping men with APC around for many years without the all too common nasty side effects of modern GnRH drugs. My father and his two brothers lived into their late 80's with the help of DES...all had RP's in their 60's and experienced BCF (bio chemical failure, disease recurrence).
Estradiol is the most potent of the three major estrogens and when administered transdermally, it greatly reduces the risks of CV events that eventually terminated the use of oral estrogens for PCa
If any of you are not familiar with the mode of action by which 'flooding the body with E2' lowers T, perhaps this oversimplified explanation may make a little bit of sense. Charged with regulating the endocrine system via data received from E2 receptors-hypothalamus, the tiny, pea sized pituitary gland sends signals to the testicles to maintain normal levels of T. When E2 levels become abnormally high, the pituitary sends messages to the testicles saying something like this: "Hey guys, I'm not sure what the hell is going on here, but I believe you are the ones responsible for this mess by producing too much T, some of which is subsequently converted into E2. That being said, it's time to get your act together and slow down the production of T to get this situation under control. Regards, The boss."
If any of you gurus find my explanation to be incorrect, please apprise...I won't be offended!
I think it would be interesting to hear from all of you that are currently using or have previously used tE2/E2 EXCLUSIVELY. If you are amenable to this request, please share with us any positive OR negative experiences you may have. Any experience with DES may also be helpful.
Thanking you in advance...cheers,
Ron
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I have been extremely interested in your therapy. I am on the side line. It’s time for me to use something and obviously I want to make the right decision. I do not know if I have Mets or not. Still imaging scans are not clear. Will your therapy works even in the case of Mets as well as Other more potent ADT drugs? I have never been on any form of ADT but need to make a decision and start something this summer. Thanks for your thoughts. Stay safe.
I have 5 bone mets and bioidentical Transdermal E2 gel/cream has been working for me going on almost 1-year. Compared to Lupron ADT hell, I would not think of going back to Lupron. Getting the same results with far less side-effect and better QOL and at a fraction of the Lupron $5,000 or Eligard $1,800 per injection.
Read the 2019 NCCN Guidelines for Patients with Prostate Cancer extensive summary of everything you need to know about all of your options for prostate cancer treatments. Good reference to have and read.
They make a minor mention of "Secondary Hormone Therapy" in pages 45-47 listing Estrogen. Download the PDF.
The 2019 NCCN Guidelines for Patients mentions DES as a treatment option on page 45 which Herman refered to. I think this guideline needs an update. Wikipedia writes: "The last remaining U.S. manufacturer of DES, Eli Lilly, stopped making and marketing it in 1997."
I have read through some of your history and I certainly would try the tE2 therapy before subjecting myself to other more expensive and aggressive treatments/drugs. I'm not a doctor, just a guy who is having great success with tE2 gel and if I knew three years ago what I know now, I would have tried the gel before consenting to sacral lymph node excision. Even though the surgery reduced my PSA by ~60%, it continued to rise until I started on the tE2 regimen. I believe that "Tall_Allen" was correct when he mentioned that the 68Ga-PSMA-11 PET/CT scan that I had preformed in Melbourne, AU most likely only identified the larger (>4 mm) mets and removing those would leave the smaller ones to continue growing.
In addition to a rising PSA , my ALP was also climbing above the maximum range which was most likely an indication of abnormal bone activity. The gel has also brought that back down to well within the normal range.
Richard Wassersug (the tE2 guru) believes that the gel is equally as effective as the costly and frequently nasty GnRH drugs with minimal side effects.
With your most recent PSA of only 0.86 I think you are a good candidate for tE2 therapy, if you don't have a big problem with the boobs which should be the only side effect. After all, you can always stop if it doesn't work for you.
I would recommend the gel (if you can get it) over the Patch since it should be cheaper, causes no skin irritation and is as easy to use as applying sunscreen. Some men have used E2 cremes; however, I think that the gel is more effective. One of our comrades, "Appraiser" found it on the NET for $10/tube at 'IVF Pharmacy' in Israel. I don't know if he or anyone else has ordered it from them...would be interesting to see if they deliver as advertised?
I may send a bunch of it back to my daughter in IL so that she can supply some of the guys who are having difficulty finding the product. My latest cost was $13/tube plus an exorbitant $130 DHL shipping fee on 24 tubes.
There are a number of men on this site that have posted their experiences with tE2. I strongly recommend that you read through them...most are very encouraging.
My best to you with whatever path you choose to take. Don't hesitate to ask if I can help you in any way.
Just wondering if you could comment on the actual ways to apply the gel and where to apply it, How do you actually measure how much to apply, etc. I’m getting ready Just in case the DES fails
Were you able to obtain the Oestrogel and if so where and how much?
*I just recalculated my dosage to the following:
I started out applying a bead on the ruler/applicator 3 inches long which is slightly less than 2 g of gel (the way that i apply it) and yields about 1.1 to 1.2 mg of estradiol. I apply it to my inner thighs, lower abdomen and around my spine below the waist. I did this once per day and gradually increased my dosage to twice a day which is giving me about 2.25 mg of E2/day. I started out checking my PSA, E2, T, and ALP about every six weeks until I was able to get my PSA down to <0.1. At that point I checked my blood every three months and made slight adjustments to maintain a PSA that I was comfortable with. Richard W. does not think that being precise with the daily dosage is all that important so I don't worry about the bead always being consistent in size. I have a photo on my intro page showing the approximate size of my dosage.
My T and E2 numbers are sometimes a bit confusing since they do fluctuate. My main concern is my PSA so I don't pay a tremendous amount of attention to the others. Richard and I have discussed these fluctuations and we really don't have a valid answer; especially since I don't vary my dosage significantly...the important thing is that my PSA is relatively low and constant. If you look at my T levels below you will see that in late 2019 and early 2020 it had increased slightly and my PSA also went up slightly in February of 2020. In August of 2019 I reduced my dosage slightly which didn't affect my PSA until in February. At that point I increased it by about 10 to 15% which brought my T and PSA down again. It appears that for me ~2.25 mg is about the best amount.
I had read somewhere that decreasing your PSA slowly had better long term results than a rapid reduction.
T levels: ...................................PSA's
4/01/2018 - 455.................0.71...Started on the tE2
Very helpful......No I haven’t got around to getting the prescription from my Doctor yet. Waiting to see what my PSA is In June......for some reason my PSA has been crazy lately. After maintaining a .6 PSA for roughly 5 years on .5 mg of DES in January it jumped to 1.5, in Feb it went to 1.78 then in March it went back down to 1.4, then on May 1st to .8.....I did however go from .5 mg to 1 mg. I’m hoping it drops a bit more but wouldn’t be surprised if it’s starting heading up again....I have to say all the time I’ve been on the DES my testosterone has been stayed around 500. I’m kind of an anomaly I guess considering I’ve had a Gleason 9 cancer diagnosed in 2004. Some people say I’m playing with fire but to be honest after 17 years I wouldn’t have done it any other way. I just didn’t want the conventional side effects
I did have laparoscopic surgery In 2004. I’m still working on my batch of older DES but there seems to be a problem getting it these days. I’ve talked to a couple of compounding pharmacies can’t seem to get it anymore
As far as the oestrogel., I did see it on eBay for $180 a tube (ridiculous) also saw estrogel at some local pharmacies for $120
What thieves! Maybe I should try selling it online; however, the shipping from Thailand is expensive. I recently sent 24 tubes to Florida via DHL for $130. Had to tell them it was cream since they won't ship gel.
Just got an email from the international pharmacy informing me that I could order up to a 3 month supply. Can you tell me how long a tube lasts you so that wHen I talk to my Doctor we’ll have some idea on how much to order
Correction: Richard and I are using about one tube of 'Oestrogel' every 3 weeks. If it is something other than 'Oestrogel', I have no idea how much to use. Are you ordering it from 'IVF' Pharmacy in Israel? I strongly recommend that you use PayPal in the event that they don't deliver as advertised. 'Herman_PSA' and another guy on our forum had bad experiences with international advertisers. Please keep us apprised...hope they come through.
I’ve been using estradiol patches for 15 months. But I also take dutasteride, metformin, rosuvastatin and celecoxib which I’ve taken since 2015 or prior.
So true, I feel relaxed and wonder where is that crazy rat race to earn more and collect more things. My neighbors seem relaxed too these days..lot of them are visible walking on side walks in the community.
The guy up there is probably giving a message to us to calm down and live simpler,more peaceful lives. Before simple life used to seem luxury..not anymore.
Hiya Ron thanks for your input. I can't believe almost a year has passed since I started on the E2 as my only treatment thanks to your advice and encouragement. So far my PSa has seen a steady decline to 0.16 - I'm due for another test soon whereafter I'll post the results. Firstly my quality of life has improved remarkably - gone are the debilitating hot flushes, depression and mood swings etc. Secondly as I'm paying for my treatment myself I've saved a neat dime or two.
There is one question I have that despite limited research I've not been able to find a conclusive answer to. In the event of not being able to source the gel, how about about using a similar one? For example I looked a a research paper that compared Premarin to the "Bassins" Estriadol transdermal gel - it seems to contain E2 also and is fairly similar in make up.
My very limited knowledge about taking estrogen for Pca control meant that long term use of female hormones meant I would grow boobs if I used the female hormone. Not one doctor suggested I take E.
ADT has not caused any CV weakness, and during the 11 hours I spend cycling around each week all year round, nobody over 65yo has overtaken me and I am a testosterone free man, have had ADT since 2012, and have fabulous fitness levels compared to so many other 72 yo men with full strength T in their bodies.
Meanwhile, I spoke to my onco today.
Psa is now 10, rapidly rising, so I'll have 7th PsMa scan 10 June, and maybe FDG scan if needed, and then maybe have more Lu177, and ADT will continue, and while I have no symptoms of any Pca, I'll keep cycling.
Doc agreed to refer me on to get more Lu177 if scans show it is likely to work again.
Thanks for your post...other than a rising PSA, it sounds like you are doing quite well. Hopefully the Lu177 will knock that back down. I am curious as to whether the E2 would reduce your PSA from 10? Maybe Richard W. will reply to this.
Wishing you another 20 years x '572' annual hours of cycling!
When an older man has female hormones pumped into him, it seems to me it shuts down his testosterone production, and his body tries to become female. I dimly remember ppl talking about this when I was young. Transgender girls who were born male may have balls and dick removed and then take estrogen to become females. It seems to me the normal ADT of Lupron, Lucrin, Eligard, Zolodex et all just shut down the balls, and have no feminizing effect, and these ADT drugs do the same as having balls removed, an op that most men just don't like, so they buy the drugs at aud $5,000 a year which are really castration drugs. Medicare funds this for me so since 2010 I have cost Medicare $50,000 and it would have been much simpler to have a single simple castration operation, and this was standard practice for men with any troubles with early Pca or BPH, because the swelling in PG went down and they could piss ok again. The days of having sex were usually long gone. Of course the castration op didn't fix their problem for very long and if they had Pca, it spread, and killed them and almost no known chemo worked.
Whether female hormones would ever have lengthened their life is unknown.
It may have worked on some men and not others. For me, if I stopped ADT, my balls would probably never turn on again, but I won't take the risk because afaiak, testosterone is still my enemy. My doc thinks that the rise in Psa now is due to Xtandi failing to work at all. I've been taking it for 13 months, so its about time it began to fail, because that's what these type of drugs do, they suppress Pca for awhile, but don't kill Pca.
With a rising Psa, its possible my taking Xtandi now could increase my PsMa expression which may give a better result when I have a PsMa scan in 2 weeks, so thus make more Lu177 more effective. My onco will be talking to docs working for Theranostics Australia, and to Prof Emmett who knows a lot about Xtandi and Lu177 effect from her research last year on having Xtandi throughout a course of Lu177.
I may need to have an FDG scan as well.
My onco is on the ball, and wants to get me good treatment where he can asap.
It sounds like you are in good hands...hopefully the PSMA scan can locate the source of your rising PSA and increase the efficacy of the LU177. I assume you are in Sydney.
I live in Australian National Capitol Canberra, Canberra, 300km south west of Sydney, so its not difficult to travel to Sydney to get the special nuclide treatment with Lu177.
Another PsMa scan will tell me and docs what is best plan to go forward; I may need FDG scan as well. All high falootin stuff that was not available here before 2015.
If you get a chance can you check with your local pharmacy to find out if they sell 'Oestrogel' by Besins in France, and if so at what cost and is a script required?
Someone online should sell it without needing any script. but exactly what you might be buying would be in doubt.
It raises estrogen levels in women enough to avoid the worst effects of menopause.
I dated a 57yo lady in 2006 who had bad case of vaginusmus and nothing could be inserted without painful reaction, but with oestrogen cream her fun parlor came back to life because it wanted to re-open for business with Rodger.
So estrogen is important for vaginal function for sex.
But it may cause increased speed of penile atrophy in men, ie, the female hormone would try to dismantle Rodger who is not a female sex organ.
Maybe a man grows breasts as well.
The emotional disposition and ability to relate to any man did not improve with estrogen added and she remained too "difficult", and she didn't know how to pay her share of costs at a restaurant or cafe, despite earning more than me, so I quit the relationship as gracefully and politely as I could. She got angry, but finally got the message when I said I'd prefer to ride my bicycle than ride her. I could not afford her.
Her menopause had begun in her thirties, and she has dyslexia, and bad temper, and has depression, and could not ride a bicycle. She could swim quite well, better than me though, but all not enough sustain desire.
Pca can cause big desire problems in couples for both men or women.
But I observed during my life that many couples abandoned having any sex once they had enough children, and both became ugly and plain undesirable. The sparks of joy disappear. I never got as far as having children, because women had other plans like travel and escaping domestic life and commitment. So when I could not have sex any more due to ADT, there was no point in trying to avoid ADT side effects, and I doubt estrogen would have done anything good for me. Nobody said it would. I have not read anywhere that estrogen significantly reduced their steady increase of Pca growth.
This is a family based chat group, with sensitive and easily offended ppl attending who would be unable to talk about Sex, Politics and Religion at any dinner party, and most definitely never discuss money anywhere. Every man has a servant called Rodger, who really makes the man his slave for anything up to 70 years for a very few men. Fanny, who is a servant of all women also is a woman's boss for lot of her youth, and with remarkable ease Fanny she controls much of what Rodger and man-servant try to do when Fanny's boss momentarily lets down the drawbridge at the palace, or opens a door in a crummy apartment on Poor Street and invites the male assault on Fanny.
I was told about 57yo ladies. I had been advised to expect a pile of female dysfunctions that will be so opposite to how the woman was some 25 years before, when it may have seemed the woman just could not ever get enough of Rodger, or Big Jack, or Harry Honker.
Somehow, ppl want the good old past to persist, but no, it just won't, as all male things fail or are destroyed by bad habits and doctors' zeal, and a man becomes a feather duster, and not like the rooster crowing about the good time he had with the chooks last night.
The older I get, the better I was, but so darn what ? I do just like a bike ride, and peace and quiet of a craft workshop, and no female ordering me about.
About 30 years ago I got a brilliant inspiration to write a book called "50 reasons why I didn't get laid last night", but then I thought not one book would be sold. Nah, what ppl want is "50 ways to make sure you get laid tonight" but of course we all know how useful such books are. Fanny has a mind of her own, totally non-predickable and Rodger is always over eager, and gets a man to put both feet in his mouth when he tries to say something charming. So I gave up ideas of book writing, and instead cobbled up a 65MB website about audio technology. There are about 10,000 million male followers of my little website, and two women, with queer sexual characteristics, because both are quite brilliant about electronics, including all the digital stuff, that has a mode of working far more complex than any normal woman.
I think there's a huge number of ppl in world who just find mating with opposite sex impossible, so they retreat into intellectual pursuit, and nightly invite their right or left hand to please their own Rodger or Fanny. Naturally, this is never to be spoken about.
Ron, My oncologist does not want to prescribe the Estradiol plasters as she thinks it won't work. I have had all kind of treatments including HIFU, Brachy and ADT like Zoladex and Xtandi. My PSA went up from 12 to 36 in two months and I have about 5 metastases of which only one is a bone metastasis. Do you think these Estradion plasters might help? My oncologist wants me to start the Chemo treatment Docetaxel a.s.a.p.
Can you send more info, e.g., age, year of dx, Gleason score and any other pertinent info either here or in a private message. I would like to share your history with Richard W.
In september 2006 my PSA was 15 and in may 2007 I was finally diagnosed with Prostate Cancer with a PSA of 45 and a Gleason score of 4 + 3 = 7
In november 2007 started with Casodex 50 mg/d.
On 20-11-2007 PSA: 16.
On 26-11-2007 HIFU in Antwerp as this was not yet available in the Netherlands.
In october 2008 an ERC MRI discovered a recurrence in the Prostate. Took biopt: Gleason score 4+4=8
A scan indicated that there were no visible metastases.
As from november 2008 Casodex 100 mg/d. PSA dropped to 0,7
In april 2009 5 lymph nodes were removed and tested clean.
In august 2009 I had a Brachytherapy in Utrecht University Medical Centre with 50 implants.
September 2009 : PSA 3.4
In october 2010 MRI indicated recurrence as well as lymf metastases.
In december 2012 start Zoladex.
Several years with PSMA PET scans and Zoladex injections. The PSA fluctuating from 9 to 14 started to rise in februari 2018
Started with Xtandi in march 2018. PSA dropped to 2
Continued with Zoladex
Jun 2019 PSA: 9.5
In July 2019 stereotactic radiation of 5 metastases. Successful.
However in december 2019 th PSMA PET scan showed new metastases.
On 20 jan 2020 PSA: 9
On 14 apr 2020 PSA: 35 !
Th oncologist wish to start a.s.a.p with the Chemo treatment Docetaxel. There was some delay due to the Covid-19 . Moreover we had some discussions on Lu 177 in Germany as it is no (yet) covered by the Dutch insurance.
Wow...you have really been through a lot in the last 14 years. Are you experiencing any symptoms? I question the efficacy of E2 after all of your treatments; however, we have some extremely knowledgable people on this forum that I believe can help you. Among them are: 'Tall_Allen', 'Richard Wassersug', 'Nalakrats' and 'pjoshea13' just to name a few. I'm hoping they will reply to this since I have listed their user ID's.
Quietly reading about this approach. I'm familiar with the path of ADT treatment. Does Estrogen gel take one down a similar road with less side effects?
My layman's opinion is yes and yes! When I ruled out conventional ADT due to cost (I have no ins here in Thailand) and probable side effects, my urologist Dr. Robert Flanigan (who I have tremendous respect for) at Loyola Hospital in Illinois suggested that I try to find DES since that was what he had prescribed with favorable results back in the 70's and early 80's.
DES has been shown to be effective when administered to patients after other forms of ADT have failed. Since E2 is an estrogen and its pathway is similar to DES, my thinking is that its efficacy should continue for a relatively long time before the body builds up a tolerance. Richard Wassersug has been using tE2 for over 15 years and still has an extremely low PSA (considered undetectable by 'some' standards). Many men continued to benefit from DES even after 20 years.
I remember that Dr Myers used the estrogen patches rather frequently. After his retirement, I went to Dr drake along with a number of other former Dr Myers patients. I asked Dr drake about these patches and he said he found some of these users had developed blood clots. Guess that’s why he wasn’t so keen on their use.
A few months ago when I reduced my usage slightly, my T went back up to 99 and my PSA rose to 0.012. However, T can vary quite a bit before it has a significant affect on PSA. According to Richard W. it takes awhile for the PSA to respond to changes in T levels.
Yes Bob I did increase my dosage slightly...I'm guessing maybe 10 to 15% which brought both my PSA and T down. However, my E2 has been all over the board as you can see in this chart. Very confusing to say the least.
My husband is stage 4, mets in torso, gleason 8. Not in pain. He has not taken the newer drugs with the stronger side effects and doesn't want chemo. We have showed this to our oncologist and he is okay with it but won't let us do the gel or cream. He insists why not do the 1 mg pill of estradiol. He has been on the meds for 6 weeks now and will have his first blood test next week. I really wanted to follow your protocol because it is working. I like the idea of not having to worry about blood clots etc. The pills will still cause that. I will keep you updated and maybe do a change
The med/s that he has been on for six weeks is only the 1 mg daily dosage of E2, correct? I don't understand why your oncologist will prescribe the oral E2 and not transdermal E2?
1 mg of E2 is a relatively low dosage and IMO shouldn't generate a substantial risk of clots. We really need to look at his PSA, T, and E2 levels when he receives his blood test results next week. What treatments/therapy has he received so far (if any) and do you have his most recent PSA?
This summary is taken from "Appendix I - Results from the PATCH trial so far" PATCH Protocol Version 12.0 August 2019. My apologies if this has already posted. Lends strong support to the consideration of tE2 as a primary treatment protocol alternative.
"There have been some encouraging results from the PATCH trial to date (n=875 patients recruited up to 6-Oct-2015)
*Transdermal oestradiol achieves similar castration rates as LHRH
*Risk of cardiovascular morbidity and mortality is similar in the two arms, suggesting transdermal oestradiol avoids the cardiovascular risk seen with oral oestrogen.
*The bone health sub-study showed patients on transdermal oestradiol avoid the loss in bone mineral density associated with LHRH
*Patients treated with transdermal oestradiol have a number of improved quality of life outcomes at 6 months compared to those on LHRH, particularly less fatigue and improved physical functioning.
*Transdermal oestradiol results in more favorable metabolic profiles than LHRH.
* In pre-planned confidential interim analysis in Jun-2013 (n=638) transdermal oestradiol met the pre-specified criteria for non-inferiority compared to LHRH based on progression free survival ( leading to the phase III extension of the study)
"Male patients either with newly diagnosed advanced prostate cancer or previously treated
with radical radiotherapy or surgery but now have a rising prostate specific antigen (PSA) are
eligible (for further details on eligibility see Section 4.0). Patients will be excluded from the
study if they have a significant history of CVS disease or they have received prior hormone
therapy for localised disease.
The overall recruitment target for the definitive phase III efficacy evaluation of transdermal
oestradiol is around 2500 patients. This includes the 680 patients recruited in the earlier
stages of the trial (apart from the first 51 randomised before the change in patch dosing
schedule3
), as well as patients recruited to a transdermal oestradiol comparison within the
STAMPEDE trial (opened in June 2017). Recruitment is expected to last until mid-2020, with
a further 2 years follow-up prior to final analysis".
Thanks for posting this! I love reading about the potential (and actual success) of non-mainstream care that limits side effects yet still has lots of science and results to back its safety and efficacy. Ron, I think (as a layman) that your description of the mode of action was perfect.
The big problem for those of us in the US is that few MOs want anything to do with tE2 for PC. They mostly 1) equate it with oral forms, 2) are put off by the inability to micro-manage dosing, 3) are terrified it is outside the mainstream SOC, and 4) don't even understand the mechanism of action that you described above!
As you (and others) pursue input from those either using or interested in transdermal estrogen monotherapy, the following information would be useful for those (like me) that are curious:
1) Which countries seem most accepting of this therapy by the medical community, where it may be less of a DIY therapy? (I know only of the PATCH trial in the UK... they seem to be on the cutting age of clinical trials because the nationalized system could save TONS of money with this, if it ever goes mainstream... bad news for big pharma.)
2) In any of these countries (especially the US), which specific docs (whether MOs or not) are actually willing to work with patients on a transdermal E2 protocol? If we have names, we have at least the beginning of an ability to influence and educate other docs who are either non-believers or deny this therapy even exists.
3) In which countries does gel (or patches) require prescription and in which is it readily available OTC, or by mail/internet without worrying about breaking laws? Are there specific brands/doses to look for, or to avoid?
4) What is the best way to convey "proper dose" to a patient or a doc who is unfamiliar with it? I know that you and RW do it "by feel" to some extent, and that RW says just to get to E levels in the range of a pre-menopausal woman, but many docs may not be comfortable with this lack of specificity (and the wide range of your own reported E levels).
My urologist prescribed estradiol patches for me with no problem. I use only (3) .1 mg patches changed weekly . Sandoz is the pharmaceutical who sells them.
Thank you for your kind reply and well taken comments. I will make an attempt to answer your questions to the best of my ability; however, I need a little more time to compile some reliable info for # 1 and 2.
In reference to # 3, I buy "Oestrogel" OTC here in Thailand without a script. I believe that most or all estrogen pharmaceuticals in America require a script. This particular product that is made in France by Besins is very difficult (if not impossible) to find in the States. There are other E2 cremes and perhaps gels available; however, I have no experience with them. One of our comrades, 'Appraiser' replied to my previous post (Update: 25 months....) regarding availability of the gel at US pharmacies and online, but getting it from any of these sources is questionable. Richard W. said that he has to have a prescription to buy it in Canada...Oestrogel is the only product that he and I use. I'm checking with some of my friends in other countries for availability.
Regarding # 4; I just replied to 'Appraiser' who had similar questions about dosage and application. Hopefully that will give you some guidelines.
Sorry, I just recalculated my dosage reply to Appraiser's question. One tube lasts me about three weeks so I divided 80 g by 21 which comes out to slightly less than 4 g/day. That equates to about 2.2 mg of E2/day. Obviously it is difficult to compare the gel to the Patch using Break60's numbers.
Regarding your inquiry of tE2 users here, I did my adjuvant ADT with PLN RT using PATCH protocol E2 of four patches 0.10 mg/24 hrs biweekly patches and changing one patch per day. Also took Tamoxifen 10 mg. Felt just fine with no perceptible SEs. However my T level was coming down slowly and still not castrate after 2 weeks during the RT. So I requested a single injection of 120 mg degarelix which promptly brought T to <20 in 24 hour!
And still I found that I felt great with the combo: no hot flushes, no fatigue and no mental fog, etc. Dropped down to two patches for the duration and still was fine. I suspect that just one patch or equivalent gel combined with the degarelix is a winning combo for me.
Furthermore, after stopping the E2 and no more Degarelix I was still castrate, T <20 at three months after the single injection. So monthly dosing does not appear to be necessary.
I've been on Estrogen patches fro three years now. Following RP PSA was 3 and climbing. At the time the RP surgeon told me the only option was ADT and get to get really fit as it would probably kill me from cardiac arresrt.
I immediately left that Cancer Centre and transferred to one closer to home and a very responsive and open minded Onc Dr. I provided a number of medical journal articles which he read, we discussed possible risks and wrote me the script. The reason I was not interested in ADT drugs is bad cardiac arrhythmia and daily night sweats in a friend of mine and in the clinical documentation of ADT family of drugs.
When I started in April 2017 PSA was 16.9 and rising, T was 13.9. Now PSA is pretty steady at <.008 or pretty much below the radar and T is <.1 also below the radar. No night night sweats or heart issues nice little boobies but hell I'm 68 the wife left years ago and the dog doesn't care. I was getting monthly bloodwork to monitor progress and fine tune dosage without having to go see my doctor.
I use Novartis Estrodot 100 patches. I started out using two at a time and changing every other day but decrease in PSA stopped so increased to four patches and change two each day. As Estrogen is not on the list of Standard Cancer Formularly in Ontario Canada and no private insurance plan it costs me C$216 and month. Not cheap but very effective.
I was pursuing an application through my Onc for coverage as special exception and that was rejected outright without chance of appeal. Apparently it is the drug company which must apply for inclusion on drug formulary which they will never do and undermine their very lucrative contract for all sorts of approved but dangerous ADT drugs.
Since castration-resistant prostate tumors will continue growing despite low levels and even in the absence of androgens, I kinda doubt that the efficacy of E2 therapy will be any different than that of conventional ADT drugs. However, I do remember reading somewhere that some patients who had built up a tolerance to GnRH drugs, actually had a favorable response to the old oral synthetic estrogen DES. I don't recall the article mentioning whether the patients were CR or if the conventional ADT drugs just ceased to reduce T to castrate levels. I'll try to find more info and if successful I will apprise.
TB, I've done a bit of research regarding estrogen therapy for APCa and whether it can be helpful for men who are CR. Some of this dates back to a few years ago; however, I don't believe that more recent findings will conflict. This info is in reference to DES which we know increased CV events due to the first pass hepatic metabolism phenomenon. Transdermal E2 (tE2) unlike oral estrogens is a much safer therapy since it is absorbed directly into the bloodstream through the skin. DES and E2 are similar in that they are both estrogens; however, E2 is the most potent of the three major estrogens.
I wasn't able to find much info relating to estrogen therapy's efficacy in treating CRPca, but perhaps you may be able to dig up some articles that I missed. In the last study (marked with a asterisk) they didn't say if either the CVD or the DES would have been effective if used as monotherapy.
Here are some findings from my search:
Estrogens. Some synthetic versions of female hormones are used to treat advanced prostate cancer. In fact, they were one of the early and most effective treatments used for the disease. However, because of the increased cardiovascular risks mainly associated with oral versions, they're not used as often anymore. J. Brantley Thrasher, MD, a spokesman for the American Urological Association and chairman of urology at the University of Kansas Medical Center, says they're usually used only after initial hormone treatments have failed. Examples of estrogens are DES (diethylstilbestrol), Premarin, and Estradiol.
Study 2, which evaluated lower doses of DES, demonstrated that 1- and 5-mg doses appeared to have equivalent effects on reducing prostate cancer mortality despite the fact that the 1-mg dose did not reliably achieve castration levels of testosterone.
*Castrate-resistant prostate cancer (CRPC) is the main cause of prostate cancer (PC) morbidity and mortality. Newer therapies have only modestly improved survival. CRPC patients’ various comorbidities mean one must treat them cautiously. Cyclophosphamide, vincristine, and dexamethasone (CVD) therapy has a favorable risk-benefit profile, and diethylstilbestrol (DES) was used widely in PC. The patient we describe responded remarkably to combination treatment with CVD plus DES. The 77-year-old man had fulminant CRPC with multiple comorbidities and bony metastases in March 2008. In May 2008, his prognosis was dismal: performance status score, 4; pancytopenia; 51 × 109/l platelets; abnormal coagulation profile consistent with disseminated intravascular coagulopathy; and cranial images consistent with dural metastases. We administered one dose of CVD (cyclophosphamide [300 mg/m2 IV], vincristine [1 mg IV], and dexamethasone [0.75 mg PO b.i.d.]) plus DES (1 mg PO b.i.d.). He responded quickly with no clinically significant toxicity. His performance status improved and platelet count increased to 89,000 × 109/l. We administered maintenance CVD (cyclophosphamide, 150 mg/day PO for 21 days every 28 days; vincristine, 1 mg IV weekly; dexamethasone, 0.5 mg PO b.i.d.) plus DES (1 mg PO b.i.d.) for 5 months. In January 2011, nearly 3 years after his initial treatment, he remained alive and well. CVD plus DES may help selected patients with advanced CRPC who are too ill to tolerate or benefit from other therapies.
DES has also been widely used for PC. In patients with non-CRPC, it suppresses the hypothalamic-pituitary-testicular axis and testosterone production.24 According to published reports, DES additionally suppresses adrenal androgen production; this may be the mechanism underlying its usefulness in treating patients with CRPC.24,25
These facts led us to try CVD plus DES as a last resort in the case of this patient. His DIC improved substantially, as evidenced by normalization of his coagulation parameters. He also experienced notable improvement of the metastases, including the cranial dural lesions (Figure 1b), and the pancytopenia resolved soon after treatment was begun. His overall clinical picture improved remarkably as his performance status score improved from 4 to 0. Despite his devastating clinical status, he tolerated this treatment extremely well, with no clinically significant adverse effects.
Conclusion
From our success with this patient, we conclude that CVD plus DES may help certain selected patients with advanced, fulminant CRPC who have multiple bony metastases, dismal performance status, altered mental status in the setting of dural metastasis, and frank DIC accompanied by bone marrow failure. Such patients are too ill to tolerate other therapy, especially standard chemotherapy, which may cause more harm than good. This CVD plus DES treatment is advantageous because it is generally well tolerated, causes minimal bone marrow suppression, and may improve patients’ overall performance status, quality of life, and, possibly, clinical outcome.
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