Bipolar Androgen Therapy (BAT) is the alternation of Androgen Deprivation Therapy with high doses of testosterone to reset castrate resistant prostate cancer to again become sensitive to Androgen Deprivation Therapy.
While it is counter intuitive, it is supported by small clinical trials. See:
This Is s pretty small trial, with only 10 patients. But it appears to confirm the effectiveness of using bat to retrospectively reset castrate resisant prostate cancer.
It was limited to patients who had been on androgen deprivation therapy for at least 12 months. That sort of makes sense.
Poshea is currently using Bat prospectively to prevent castrate resistance from occurring. He has been using it I think for about 5 years and appears to be satisfied with the results.
My question is: Why Not to Use Bipolar Androgen Therapy (BAT)?
After being on Androgen Deprivation, why not some testosterone? Why not at least try it?
Has anyone else here other than poshea tried Bat, or considered trying it?
I have thought about that. If it is alternating every other month, it seems like it would be possible to test it for its effects on you, and stop it if it gets out of hand.
I recollect someone on this forum tried it. Their PSA jumped, and they jumped off of the testosterone right away.
Someone here said that it only works for 20% of the patents. But I forgot to ask them what study they were reading from.
In the study above, it seemed to work for 10 out of 10.
I think it probably helps if you find an oncologist with some experience doing it, to benefit from their multiple experiences with it.
But in the end, it seems worth it to give it a one person tentative trial when you look at the alternatives.
Pretty much all the alternatives for treatment of castration resistant prostate cancer have side effects that, were they to stand on their own, would be considered very serious conditions on their own. They are acceptable only because the alternative is a very painful death from prostate cancer.
It should only be done in the context of a closely monitored clinical trial, where the patient is aware that it might hasten his death. It is not at all clear, at this point, that there is any benefit in terms of survival, even among those who appear to respond. We also don't know yet how to choose patients who respond and how to weed out patients who get worse.
2. I notice it has a 2018 comment about a BAT clinical trial in Colorado that excludes anyone who has been on Xtandi. Do you know anything about that trial?
I only know what I read on the link. They are trying to see if it can extend the enzalutamide-sensitive phase (compared to historical controls, I suppose)
I need some help here. If one is currently castrate resistant with ‘T’ at very low levels, let’s assume below 10, while on ADT,,,, how would bringing ‘T’ up to let’s say 1,000, make one’s PCa worse?
It appears to me that the ‘bad’ resistant cells care not a wit about the amount of circulating ‘T’ levels as they are manufacturing their own or have learned to live without it, although perhaps the far less dangerous ‘T’ responsive if any remain, might have a field day.
Normally I would tend to believe that most men or their Physicians would not experiment with BAT unless Castrate-Resistant
I believe my question boils down to this. Are there any evidence based trials that confirm any of these theoreticals?
See the link I posted above. One of the ways in which castration resistance occurs is through amplification of the androgen receptor. This makes it exquisitely sensitive to even the smallest amount of testosterone. That's why Lupron (or similar) is always continued after castration resistance sets in.
Here is what I believe - partly because of my 15 year experiment. Traditional ADT (i.e. Lupron, etc.) selects for cells that are difficult to manage. Modern ADT (i.e. tratitional ADT + Zytiga, Xtandi, etc.) selects for cells that are even more difficult to treat. Testosterone [T] reinstatement can shock some cells into apoptosis, but the success rate will be lower in men who have had a lot of treatments.
From the start, I did not want to be on ADT for as much as a year, but I knew that shorter periods of castration in the intermittent ADT [IADT] setting did not lead to long ADT 'vacations'. When I finally had to be on ADT, I chose 3 months as my maximum.
I really enjoyed those 3 month vacations with T at ~1,000 ng/dL. But if I had known of BAT, I would have opted for monthly cycles.
When BAT is used at the start of ADT, it has the maximum chance of being effective, It isn't something that I would save for when all else has failed.
Note that BAT is not IADT. It is a form of ADT, where T is given to shock cells back to their original state. It is a way of dealing with the short mean-time-to-failure of traditional ADT (18-24 months).
-Patrick
cesanonin reply to pjoshea13
Hmmm, so summarizing what you have learned:
1. Short periods of castration, lead to shorter periods of castration vacation.
2. You think one month on and one month off is optimal, at least for you.
3. You bipolar androgen therapy (bat) where you use testosterone during the castration vacation is more effective if used early before too many cycles of intermittent adt.
Question: Why exactly do you favor short we cycles of intermittent adt over longer cycles? That seems counter intuitive to me?
pjoshea13in reply to cesanon
It all comes down to not giving PCa cells time to adapt. Adaptation leads to treatment failure.
The T 'vacations' are not really vacations. A single T shot to shock the cells that have had a couple of weeks with virtually no T.
You mention "one month on and one month off". The BAT cycle occurs in a single month. But one month on and one month off is more attractive & might be non-inferior, or even better that BAT.
One month on and one month off might be more prudent than my three months on and three months off.
The key is that the off periods should be with high T.
-Patrick
cesanonin reply to pjoshea13
"When BAT is used at the start of ADT, it has the maximum chance of being effective, It isn't something that I would save for when all else has failed."
Isn't the whole purpose of bat, to use it after adt has failed and the prostate cancer has failed.
If it's purpose is to resensitize prostate cancer to androgen deprivation therapy, what is the benefit to using it early?
pjoshea13in reply to cesanon
I belief that its primary benefit is to forestall CRPC.
-Patrick
cesanonin reply to pjoshea13
Oh. It is not to reverse it. It is to prevent it from happening in the first place.
pjoshea13in reply to cesanon
Yes - that is where the greatest benefit should be - IMO.
One problem I ran into right away was obtaining injectable testosterone..It's a controlled substance and getting a doctor to write you a script for it is not a simple matter...
Not a good idea to use it without a supervising medical oncologist. Actually quite dangerous. And you want not a normal MO but one who is experienced using BAT.
Here is a currant study of 47 men. So far, none of them has died from BAT..Most have enjoyed dramatic declines in their PSA numbers. No one has experienced a dramatic rise..
"Researchers observed that 30% of the participants had about a 50% reduction in their PSA levels, while 40% of the men also experienced a dramatic decrease in their PSA levels."
Means 70% of participants' levels went unreported. And 60%... that's where I got lost. "reduction" and "dramatic decrease" both refer to PSA levels.... I mean, WTF?
Thanks for posting about BAT. I believe it is important for people in this forum to realize that the SOC sooner or later will take the cancer to a stage where is impossible to control. BAT and other therapies (direct treatment of metastases, vaccines, Lu 177 PSMA, xofigo, celebrex/ zoledronic acid etc) have the potential to delay the use of SOC drugs. I completely agree with Patrick's approach to treatment.
The typical response used by oncologists to refuse to do BAT, is: "it has the potential to make the disease worst". IMO, this position is not really supported by Sam Denmeade's studies.
Oncologists have been trained since birth to suppress and avoid testosterone. ADT is their most effective weapon against PC... It will be hard to turn that around..
Spot on..just finished my last Lupron injection of an 18 month cycle two months ago, still hormone sensitive and PSA <.02
Me: If I still have some PC cells floating around wouldn't maybe the next 3-6 months be the time to blast them with Testosterone when they're really Androgen starved and the effects of ADT will be wearing off?
You got that right! My MO is all ears when I explain the nuances of my BAT therapy. She always zooms her chair next to mine to discuss and look at my labs.
“If we find testosterone is superior then we would hope to move on to larger trials. Our problem is this is not a drug that is owned by a pharmaceutical company; it is generic testosterone. So moving forward is going to be difficult due to issues with finding funds to run a bigger trial.”
-Professor Sam Denmeade Johns Hopkins University School of Medicine
Dr. Denmeade presents a real and very common problem. I just emailed in a partial solution to it. I'll see if he responds. LOL
He does respond to emails, in my experience. He pointed exactly why this subject is not further explored in other academic centers. I know very well that medical investigators make careers with grants paid by the pharmaceutical companies. I have great respect for what Sam Denmeade is doing.
I agree with those doctors, "it has the potential to make the disease worse". And also that ADT has the potential to give you a heart attack. And chemo has the potential to cause you to die of an infection.
And of course, BAT has the potential to extend your lifespan.
• in reply to
So we get into the usual balancing act.
• in reply to
And as always, much of the ultimate responsibility lies with the patient.
I am pretty sure Denmeade at Johns Hopkins in Baltimore. He is often quoted on the subject. Dr. Danila at MSKCC said it was at very early stages and results had been sketchy in his experience. I did not press for further details at the time. I had newly discovered population of METS and explosive in crease of PSA. Firmagon,zytiga and prednisone and 60 days have improved my Labs. PSA down from 47.3 to 6.7 and alk/phos from 149 to 88. I am hoping for this friendly trend to continue. I will follow BAT discussion and papers closely for consideration.
After six years and many tx I’m still castrate sensitive . Being tired of ADT off and on for five years and related side effects I switched to estradiol patches last January. Side effects ,except for breast pain at first, are gone . T is below 10 and Psa is .1. A heck of a lot cheaper than ADT and more humane. This should be SOC and hopefully FDA will approve at end of PATCH trial in UK.
Estrogens in men cause the hypothalamus to release less GnRH hormones. As a result, the pituitary gland in turn releases less LH and FSH hormones and thus reduces testosterone production in the testes.
I remember Dr Myers used estrogen patches. When I asked my new dr , dr drake, about this knowing he had taken over other dr Myers patients and knew him well, he said for a number of them he had to stop the patch due to blood clot issues. I had thought the transdermal patch avoided this problem.
so what do you take to reverse this? I can't get my balls to get restarted after ADT, though the fact I was lowish T to begin with may be part of it. My estradiol readings are <15, which the test says is normal
e. (I have not tried this) A possible method to use for low dose estrogen replacement if it isn’t possible to obtain estrogen patches: The pros and cons of phytoestrogens - PMC
g. Early hormonal data from a multicentre phase II trial using transdermal oestrogen patches as first‐line hormonal therapy in patients with locally advanced or metastatic prostate cancer - Langley - 2008 - BJU International - Wiley Online Library
j. Concurrent Androgen and Estrogen Ablation and Inhibition of Steroid Biosynthetic Enzyme Treatment for Castration-resistant Prostate Cancer | Anticancer Research
I use Sandoz patches. Estradiol is estradiol as far as I know.
My intervals and tx are shown in my profile. They were short due to fast psadt so iadt wasn’t working well for me.
I don’t have a MO. Haven’t seen the need for one yet as I’m not castrate resistant. . I asked my urologist Dr Langley in Hilton Head SC ( same name but no relation to Dr Langley in UK running the PATCH trial) and he agreed with patches since he had used oral estradiol back before it was stopped due to CV events. Plus he did due diligence talking to experts like Dr Wassersug and others who Wassersug used as sources.
I don’t know Nal’s opinion on estradiol but I’ve seen it. I’ll ask him.
I’m relying on the PATCH trial results , Dr Meyers video and a white paper discussion of types of ADT and effects on the body by NIH. See
I googled to find this so I don’t know. Given that it’s inexpensive and might replace lhrh agonists no pharmaceutical company will sponsor a trial so the UK trial is the only one I know of and it’s very rigorous and will take years to complete. It’s good that NIH has looked into it. I asked Dr Meyers if he would publish something on prostateopedia his newsletter. They might in the context of another issue on ADT. He has published a utube video on it.
I read the nih article and they takes about the estrodial being less expensive than something like lupron but what I'm not clear on is whether these patches after meant as a replacement alternative to lupron or is it supposed to be used until it stops working and then moving on to lupron later, this extending castration sensitivity?
Not a substitute. I found them far superior. Test undetectable in 6 weeks after starting. Felt great mentally. Didn't notice many side effects other than what zero testosterone is going to do; regardless of how you get there. Lupron typically doesn't get T down to undetectable levels. Has bad side effects.
I started with 0.5mg daily to get into castrate levels quicker. Then I dropped to 0.2. Test was zero. Then I dropped to 0.1 and test went up to 24 ng/dl. So I went back to 0.2. Zero test in one week. Occasionally I would do 0.3mg/day but usually 0.2. Everyone is different but my doctor said that it works for every guy. All I know is that it worked for me...
One Estradiol patch does stop hot flashes when used with Lupron . But why would anyone use multiple patches and Lupron . It would be total overkill and probably dangerous. The folks running the PATCH trial are experts and are conducting a very rigorous comparison of outcomes and side effects of the two types of ADT: Patches and Lupron .
If you want to wait until the trial is over to be convinced then go ahead and use Lupron
1. You don't know that without a trial designed to determine that.
2. The trial you refer to is not designed to determine that. I doesn't investigate the concurrent use of both.
With the mutational aspects of cancer in general, there is good reason to error on the side of overkill. Inadvertent underkill promotes more mutation. Never a good thing in general, and particularly not a good thing for prostate cancer.
You’re killing me! You do your thing and I’ll do mine. If the scientists thought that adding patches to Lupron made sense why wouldn’t they have done a third arm of the trial??!!
2. "why wouldn’t they have done a third arm of the trial?" most likely cost.
Though they have their own professional/career reasons for doing the study. Those reasons are not likely to be 100% aligned with mine or yours.
They have something to prove, and they are out to prove or disprove it. For whatever reason, the third arm, regardless of outcome, is not of interest to whomever is paying for the cost of the study.
For example, if you were personally funding the study, it would appear that you might not be so interested in paying extra for that third arm? No? You just want to know if you can get by with just the estrogen alone.
Did you read the trial? They are interested in improving men’s quality of life by trying a treatment that seems to work the same but have less side effects. This is a state sponsored study. The UK that is UK taxpayers are funding it. I salute them for doing it! They have no selfish interests!
Governments don't make decisions, people make decisions.
And both governments and people are limited by budgets. They have to make choices. They chose to improve the accuracy of two arms of the study by giving up on the third arm of the study. They were obviously more interested in those two arms than in the third. They do not need to give a reason why.
However they made that choice. Whatever the reasoning. They made that choice. And we don't know why.
The reason clinical trials are required when dealing with complex biological systems and that they follow their own logic and it is a logic they don't share easily.
"It would be total overkill"
1. You don't know that without a trial designed to determine that.
It appears we don't have that trial. So we just don't know.
It sounds like the patch might be effective after Lupron stops working alone but it doesn't sound like the patch can be used first and then Lupron afterwards is that correct?
Not sure. The trial compares the two treatments to see which one is more effective and easier on the body. They’re both meant to achieve the same objective : Lower T to castrates levels. Did you read the trial ?
Seems logical to me but only if testosterone on estradiol therapy doesn't go to zero. Zytiga is a good addition. Stops a lot of the test that cancer cells make. I did Zytiga and estradiol patches (I made sure that the patches were bioidentical - climara is the one I used).
I'd love to see a trial using zytiga and estrogen patches. On conventional ADT the cancer becomes castrate resistant but I wonder if it would happen as fast or at all if testosterone was dropped extremely low.
I guess the Lupron and stomach pain makes me less sharp than I use to be but I couldn't find anything about the proposed timing of this patch and where it fits in with other treatment options with the bottom line being life extention. Im less concerned about quality of life and more concerned about avoiding cardiovascular events and life extention.
It's just another way to get ADT. I have done Firmagon, Lupron, and estrogen-ADT.My T was detectable but very low on Firmagon. Detectable above 30 on Lupron, not detectable on estrogen-ADT.
UK Patch trial shows that I am not the only one who gets superior T control from estrogen.
But it has not been U.S. SOC for over 30 years and will be a hard sell to get it reinstated. As my MO once said "if it doesn't happen here, it doesn't exist" - so the UK Patch trial does not exist.
Experience is very important in all fields of endeavor.
Whoever would supervise my Bat, I want to have as much experience with as many bat treatments as possible.
If you are setting up a chemical production line, do you want an engineer with no experience in setting up high production chemical systems?
If you are getting divorced, do you want a highly competent lawyer who has never handled a divorce?
If you are developing a real time production monitoring system, do you want a good programmer with no such experience, who has done most of their work on Hollywood movie graphics.
For myself, I want my Bat supervising Doc to have as many prior Bat patients as possible.
I am not worried that my doc will share my personal medical information with other patients. Do a search on "HIPAA".
That's why I am putting Sartor out there. The more Bat work he supervises, the better he will get at it.
And if we can develop a community of 5 or 6 docs doing it, we are all better off for it.
His book on prostate cancer (on amazon): The New Testosterone Treatment: How You and Your Doctor Can Fight Breast Cancer, Prostate Cancer, and Alzheimer' s
It's not about me Nalakrats. Between Sartor and Demeade, I am good.
There are others in other parts of the country who are not so able or willing to travel.
And thanks for the heads up on Demeade. Don't you have to be a paying patient for him to call you and give you medical advice? It would seem legally risky for him to do otherwise.
Hi, I posted this a few months ago. Maybe there are links and other interesting studies for you on the end after that article ?healthunlocked.com/api/redi...
I know some in the group have tossed the idea of BAT around previously. The approach does seem like a pig in a poke with the fear that the PC could take off. I haven't browsed the papers above where the detail is cited. Did these studies contain patients with highly aggressive PC, lets say Gleason >9-10 (as myself). Alternatively, have folk in this group with the same aggressive phenotype undertaken BAT? And with what results?
It appears to work. If you dig into the papers they have a detailed hypothesis as to why it works.
The paper I looked at had 10 non-symptomatic métastatic patients who were castrate resistant. At that point Gleason is sort of irrelevant. They all benefited from the therapy.
If you pick up something from reading the papers, please post it.
67% had GS 8-10. Metastatic burden: Bone only 53% and soft tissue 30%. Almost all with AP below UL—> means not to many/big mets on bones. PSA doubling time was not predictive for response. Best response (without flare in the 1st month) was seen with baseline PSA >50.
Also, BAT reduced total CTC and AR-V7 compared to baseline.
Herewith a draft extract from my new 3rd edition PCa book (An ABC of Prostate Cancer Today), due out November 19. I welcome comments re the text below:
The use of bipolar androgen therapy (BAT), involving rapid cycling between high and low serum concentrations, was found to be safe and resulted in responses and re-sensitization to enzalutamide in men with mCRPC who progressed after initial enzalutamide therapy, according to a December 2017 study whose results were published in Lancet Oncology.
“Clinically, metastatic CRPC that has progressed after enzalutamide treatment is minimally responsive to further therapy that inhibits androgen receptor signalling,” wrote study authors led by Benjamin A. Teply, MD, of Johns Hopkins School of Medicine in Baltimore. “Theoretically, rapidly varying the androgen concentrations between the extremes of supra-physiological and near-castrate, a strategy termed BAT, provides insufficient time for CRPC cells to adaptively regulate androgen receptor concentrations,” and thus may promote cancer cell death and prevent resistance.
The new open-label phase II study tested BAT in 30 patients. Treatment consisted of intramuscular testosterone cipionate 400 mg every 28 days until progression, as well as continued luteinizing hormone-releasing hormone agonist therapy. After progression, men were re-challenged with enzalutamide.
Sequencing tumour samples and the germline have shown that defects in DNA repair genes are common in patients with mCRPC. Research have shown that BAT disrupts DNA re-licensing and produces DNA double-strand breaks in CRPC cells. Given the emerging data on DNA repair defects in prostate cancer and the mechanism of BAT, we postulated that men with such defects may be particularly susceptible to BAT. A participant (70 years old, Gleason 9, radical prostatectomy followed by salvage radiation therapy, followed by hormonal therapy - see Figure 1) in an ongoing trial showed a remarkable and durable complete response to BAT. His tumour sequencing result supported the hypothesis that patients harbouring mutations in DNA repair pathway genes may be particularly sensitive to BAT. (His tumour sequencing revealed the BRCA2 and ATM mutations. Both of these mutations were present in the germline).
Figure1. Prostate-specific antigen (PSA) levels over time in response to the hormonal therapies indicated. (Re-produced with permission).
The RESTORE trial is evaluating BAT in men after abiraterone or enzalutamide failure. The co-primary end points were the response to BAT and BAT’s response to a re-treatment with either abiraterone or enzalutamide. Early results from the enzalutamide arm have shown a >50% PSA decline and a measurable response in about one-third of patients. BAT was well tolerated with minimal side effects. On re-treatment with enzalutamide, about 50% of patients had a greater than 50% PSA response. BAT is also able to suppress AR-V7 expression in most men with detectable AR-V7 in their circulating tumour cell samples.
The TRANSFORMER trial includes 180 asymptomatic CRPC patients who have failed abiraterone. In the study, BAT is being compared to enzalutamide for the primary end point of progression-free survival. Patients are allowed to cross over following progression to the first therapy, with an important secondary end point being PSA progression-free survival on the second agent in order to evaluate the ability of BAT to re-sensitize tumours to androgen receptor sensitive inhibitors.
The mechanism of BAT inhibition is becoming more understood as research continues. Various pointers suggest that multi-therapies that might include BAT with PAPR inhibitors, platinum agents, proteasome inhibitors or immune checkpoint inhibitors might offer improved results.
Notwithstanding the above, it is very difficult to find medical oncologists and urologists who are firstly, up-to-date with the science behind BAT, secondly are prepared to prescribe testosterone and thirdly, well experienced in undertaking this therapy and dealing with its pros and cons.
“An ABC of Prostate Cancer Today – 2nd Edition replaces its best- selling predecessor, “An ABC of Prostate Cancer in 2015”. The new edition provides the reader with comprehensive information on the very latest diagnosis tests that are available and now becoming routinely used in leading clinics, hospitals and specialist practice around the world. A leading urological surgeon who reviewed the book said: “All my registrars (interns) should get a copy of this book and fully digest its contents.” Another specialist said: “Every general practitioner (physician) in the country should read the book to bring them up-to- date on prostate cancer.” Not with standing these comments, the easy-to-read book, is targeted at the layman, and is written in easily understood language. The book provides the reader with more than 100 questions that prostate cancer sufferers should consider asking their doctors. It also details “My Journey over Four Continents to find the Best Cure”. The book (99,500 words over 344 pages) is presented in three parts: In Part 1, the book looks at what prostate cancer is and examines, in detail, PSA testing and its derivatives such as PSA density, PSA doubling time, free PSA, etc. It also looks in depth at the biopsy process and explains the increasing use of multiparametric MRI as a diagnostic tool. The staging and grading of prostate cancers are explained. Part 2 focusses on the 10 top treatments available to treat prostate cancer. Some of these treatments are broken down into multiple sub-sets. One such treatment is radiation, which is broken down into nine different forms of radiation, each of which is fully presented. Some of these, like proton beam therapy, might offer better alternative outcomes to some sufferers than more ‘popular’ treatments. Whilst the book focusses mainly on the treatment of patients with low and intermediate risk prostate cancer that is localised, the treatment of metastatic prostate cancer is also considered. The book considers diet and nutrition issues in detail and also has chapters on alternative treatments and a comprehensive cancer-fighting plan. This part of the book concludes with a chapter on the all-important prostate cancer support groups. Part 3 of the book details my consideration of various treatment options, my visits to three urologists and a radiation oncologist, my treatment selection process and my subsequent proton beam therapy treatment at the National Cancer Centre in South Korea. What the book spells out, is the need for a newly-diagnosed prostate cancer sufferer to take charge of their own destiny, by learning as much as possible about their condition and not to make quick and possibly rash decisions whilst under what I term to be the “Cancer Anxiety Factor.” The book contains an extensive Resource Listing which provides details of further reading that is available via the Web. It also provides a comprehensive Reference Listing to support the statements made within the book. Hopefully, the presentation of the technical aspects of the diagnosis and treatment of prostate cancer within the narration of the author’s own prostate cancer challenge makes compelling reading.
About the Author
Alan Lawrenson, after tertiary studies, spent almost his entire working life in the commercial side of the science industry, marketing scientific and medical equipment and running the peak industry association for laboratory technology in Australia. He also served on a number of Australian Government-initiated reviews and committees. Alan was diagnosed with prostate cancer in 2012 and wasn't happy with the treatment options initially offered by his doctors. He termed the phrase "The Cancer Anxiety Factor" that afflicts all newly diagnosed Prostate Cancer patients. A large motivation in his writing "An ABC of Prostate Cancer Today" was to provides such men with a host of alternatives that might better suit their circumstances and to encourage them to take a more proactive role in 'managing' their condition. The book describes “My Journey over 4 Continents to find the Best Cure”. His first book, “An ABC of Prostate Cancer in 2015” achieved #1 Bestseller status on Amazon on four separate occasions in 2015. As a resident of Sydney, Australia, Alan is very active as a speaker on prostate cancer to support groups and seniors clubs in NSW. The second edition of "An ABC of Prostate Cancer Today" is a completely updated variant of the original book. A key improvement of the new book is its extensive coverage of diet, nutrition and alternative treatments, which are of special importance to advanced and metastatic prostate cancer patients.
It would be incredibly easy to find testosterone cipionate online. My Father has just become resistant to Zytiga, and we have wanted to try BAT for a long long time.
Would be amazing if we could find an oncologist would support this in the Uk.
I think I’ll speak to Ed Friedman about this again !
I had a computer hang up with my last reply. I couldn't get it formatted correctly.
I had proton beam therapy in Korea. Seemed to nip the PCa in the bud. My brother is Stage 4 and is now on Lu-177 + Xtandi. Thus my focus on this topic.
Wish I had Tall Allen's knowledge and that of many from this group.
If you do BAT (as well as many other therapies) it is important to monitor your response.
Trials and studies are nice for jumping off points but IMO it is very short-sighted not to monitor yourself.
I envision someone saying, "Hey, gee, my T is 125 on this ADT drug but according to trials the average man's T goes undetectable and the gaussian spread is very small. So, all of my labs must be wrong."
Content on HealthUnlocked does not replace the relationship between you and doctors or other healthcare professionals nor the advice you receive from them.
Never delay seeking advice or dialling emergency services because of something that you have read on HealthUnlocked.
Batman BAT study updated
