I thought it might be useful if I briefly described my experience with Bipolar Androgen Therapy which has been discussed here in the past. In my case there was really no option but to source (apprehensively) “grey” market testosterone from the body building fraternity where there is extensive experience of supraphysiological testosterone. Info on how to learn intramuscular self injection is readily available as are the appropriate syringes and needles. I followed what some here call the Denmeade protocol used in Johns Hopkins trials – maintain primary ADT but stop secondary (resistant) androgen blockers and monthly inject 400mg testosterone cypionate. Continue until PSA starts to rise, then rechallenge with the secondary androgen blocker. Note this is a one off experiment and nobody should draw any general conclusions and nor is it a recommendation. There is talk of a future genetic test, but my thinking was “to find out if you respond to testosterone, Why not just do it?” Much cheaper and little downside on current evidence. But it’s an experiment of one.
Here in Australia testosterone is heavily regulated and no doctor will prescribe it to any prostate cancer patient. All my medical advisors strongly argued against it, despite knowing of the emerging Johns Hopkins results and saying they were more than interesting (but too early). The text books and students are still taught that testosterone is fuel for cancer. There is a culture of litigation and there have been cases of oncologists barred because they varied accepted treatments. There are ethics committees at all research hospitals. I didn’t see my expert advisors during my experiment. We talked openly well before.
As regards the risks of testosterone and PC there is a large data base of testosterone users over the past many decades. Morgentaler was one who drew attention to the lack of pattern regarding PC suggesting there was a band of blood testosterone in the low physiological range that provided the ideal environment for PC. Above and below it, growth is relatively suppressed until adaptive resistance cuts in. This is the “saturation model” (saturation of androgen receptors). I concluded that there is a paradigm change going on and the "testosterone is fuel" thesis is being replaced by something more complex.
As regards BAT itself there is still relatively little experience with PC and genuinely supraphysiological testosterone. A recent review by Mohammad et al emphasised this. However what is known is largely positive. There is great variation in response but most men got benefit – most notably in overcoming the resistance to their previous androgen blocker. I don’t know of any trial that tested it against bicalutamide.
My history: diagnosed 2002, radical prostatectomy, external beam radiation, ADT (zolodex), bicalutamide. All were done serially after the previous had failed. ADT continues to this day,
So: the experiment… The bicalutamide treatment lasted about a year before a rising PSA was apparent. I stopped that and allowed a month to let it wash through – having an androgen blocker while trying to stress the cancer with testosterone seemed counter productive. PSA at peak was 4.4 and doubling about every 2 months when I started the BAT. Two days after the first injection testosterone had jumped from 0.3 to 54 nmol/L. The normal range is 9.5-28.0. After a month it’s back down to near castrate levels. All advice says a PSA test after the first month is misleading (and potentially frightening). After 2 months PSA had dropped to 3.7 and after 3 months, to 3.1. It basically flatlined from there for another 5 months and then rose to 3.9, which is where I stopped the experiment and went back on to the bicalutamide. The PSA after 1 month of challenge was 1.8.
How long the bicalutamide will remain effective and whether this cycle can be repeated I don’t know. The above would indicate I am a moderate responder.
Dosage is an issue. The only trials have used 400mg testosterone cypionate and the enathate ester in similar amount. NOTE: DO NOT EVER INJECT THE PROPIONATE ESTER. It has a kick like a very angry mule. The reason for 400 mg is that the US FDA has ruled that dosage OK for humans. I increased dosage to 600mg and concluded there was no benefit. I also tried a short period of continuous supraphysiological testosterone – 2 weeks where every 2nd day I injected 200mg. Again no benefit.
I conclude that in my case, BAT may be a useful tool to manage the phenomenon of resistance and enable the effective longer use of secondary treatments after ADT has failed.
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The Denmeade protocol was 3 months of ADT followed by 3 months of TRT. ADT was with Lupron, not bicalutamide.They carefully screened patients and monitored PSA closely. About half the patients who were castration-resistance incurred progression on BAT. Until they are able to figure out who progresses and in whom progression is delayed, it is dangerous to undertake it outside of a clinical trial.
Hi - do you know where I can find the best sources of effect of Supra T on Pca? I have been running 1400-1600 for a few years on Xtandi. My dr feels it seems to change everything related to Pca.
Hi mate, I was told by Head of Research at Chris O'Brien Lifehouse that there is a BAT clinical trial happening at St Vincents in Sydney so there is definitely more than interest In this potential therapy. I was told that current thinking is that BAT is effective only against certain genetic defects. I live in Melb so it's not really convenient for me to pursue this any further I assume that if they get good results in Sydney then trial will expand to other major centers (eg Peter Mac in Melbourne).
It might be useful if at all possible, to find out the T dosage that is being used in this trial. Better than making up your own dose schedule. It would be even better to get enrolled in the trial. I would assume that you would get full genetic testing as part of the trial, this could be very useful to help you work out next treatment options.
I’m glad that you are thinking outside the box to battle this disease. However, it would probably be more prudent to do it at a center where all your vitals are closely monitored. Best wishes.
This was a fascinating post. Many PCA patients are interested in BAT. Understanding that a case report is not the same as a trial or a molecular study, and that your case may be entirely different from that of many or most men, and that you can only report limited amounts of lab work results, it's still something of great interest. BAT would seem to be one of the options that men still have when other options are running out. It's an attractive option too in that it offers relief from ADT as well as possible help with the disease. First hand information like yours, in spite of its limitations, is therefore of significant interest.
Thanks, and please keep posting as more information is gained.
Many many thanks for the responses. We are all learning here.
Tall Allen: I might have caused a confusion by referring to the Denmeade protocol. I do know of trials using the three monthly cycle of ADT/testosterone replacement therapy that you refer to and I agree the results are not too flash. However TRT will generally not get to genuine supraphysiological T levels. I was referring to the Johns Hopkins trials that used a repeated one month cycle from supraphysiological T to near castrate levels at the end of the month, all the while continuing with primary ADT (zolodex in my case, or the similar Lupron ). I agree that it would be much better to do this with proper medical supervision.
Hazard, thanks for that. My main oncologist is Lisa Horvath at Chris O’Brien but I haven’t seen her for about a year (for reasons explained in original post) and a local BAT trial was not then on the horizon. I will get in touch with her. As regards dosage most trials have used 400mg Test C and I concluded there was no benefit to me of increasing the dose. That dose once a month does not expose you to a huge amount of T as it is back to physiological levels in a week or so. The interesting question is whether continuous supra T is effective. I tried and found no benefit but in vitro and in vivo work suggests it may be for some, but no trials as yet.
Snoraste, yes a full set of tests would be good. I did PSA once a month, on 2 occasions I did testosterone to check the quality of the testosterone I acquired and about half way through did a full spectrum blood test, all arranged by my local Dr. Nothing untoward
Nalakrats, yes, switching off the ARV7 receptors is one effect that should help overcome resistance, but Mohammad et al referred to in original post think the exact role of ARV7 is still not well understood and there are a number of other possible pathways for supra T to act, either in combination or separately. Very complex. My head hurt.
Alan, yes a one off case study is hardly science although it did tell me that I responded in an average sort of way. PSA response was not huge (but significant) and the real test is the rechallenge with the previously resistant androgen blocker. In that sense BAT is potentially a management tool to extend the usage of more conventional treatment.
Thanks all. I will update when I get more results but at the moment it looks like bicalutamide is working again. There is so much we just don’t know.
Hi again. It was Prof Horvath that I spoke to at the LifeHouse you are very lucky to have her as your MO. Pls update us if you learn more about trial at St Vincent's.
We're on very similar paths. I've not written up my experience in part because the experiment is still in progress. I can add a few general observations.
The 400 mg Testosterone Cypionate dose proved inadequate to produce supraphysiological levels of serum testosterone. The target is >1500 ng/dL, and body builders often maintain 2000 for weeks or months at a time. The FAA guidance not applicable to the BAT setting. The FAA, using some criteria, decreed that 400 mg was safe but DID NOT state that higher doses were unsafe. The context of the evaluation and recommendation was not BAT or PCa.
I monitored T levels and found that 600 mg was required. Even then there were substantial month to month variations. I suspect but cannot prove that subtle differences in placement of the injection, variations in physical activity (vigorous exercise seems to release the drug from the muscle faster) and in one case a mild infection at the injection site all produced substantial changes in the peak T values and half life. My oncologist (see below) suggested a number of other variables that could affect both absorption and clearing of testosterone.
PSA rose substantially after the injection, but then dropped at an amazing rate. In one month it fell over 30 points in 9 days. If you can avoid worrying about the numbers, the trajectory is fascinating.
Truly dramatic quality of life improvements are reported by nearly 100% of men on BAT. If I hadn't started BAT I would simply have refused further treatment and put my affairs in order. ADT was completely intolerable. The monthly roller coaster ride isn't exactly fun but infinitely preferable to the slow death of existing on ADT.
You touched upon an important point about large cancer centers. They are severely constrained in what they can do. I went to several and all refused to even discuss the topic. But a compassionate and open minded oncologist at a community clinic was willing to work with me. The improvements in my quality of life and demeanor were so dramatic they are considering offering BAT to other patients who have spent years on ADT, even though they aren't yet demonstrating castration resistance.
My oncologist also supported my interest in a test of several weeks of continuous supraphysiological levels of testosterone. The theory of how BAT works against castration resistant prostate cancer cells strongly suggests that there will be benefits, but it will probably be some months and perhaps a few cycles before anything can be seen.
Clinical trials at major centers do not magically confer safety. They put you in touch with smart practitioners who are learning as they go - that's what trials are for. There is a reason that you literally have to sign your life away to participate in a trial.
The choices I've made are mine alone, and I will accept the consequences. Yes, 2 men died in a BAT trial, but men die every day of prostate cancer. The trials mostly enroll men in the final stages of the disease. The fact that it helps about 50% of these men is astonishing. Any drug that did this would be getting headlines.
If avoiding death is your only reason for living then there is no point in taking any risk at all. Might as well stay at home and hide under your bed.
Thanks again for posting this information. You are a brave man. I hope this works out well for you - and for me.
Sorry. Two brave souls! I'm printing this one for our oncologist and specialist. Back to hiding out on the couch since there's no space under the bed. Mrs. S
P.S. Nalakrats included BAT in his recommdations to us. Thanks to him. Only problem is that in the past hour my husband asked a half dozen times what BAT is. ADT should be outlawed, not standardized.
Many thanks. That is very useful information. There is great variability in responses to high doses of exogenous testosterone and it is best not to get a PSA test in the first month (can be scary and misleading). The experience of the body building fraternity seems to show that 600mg dosage is well tolerated. Some go as far as 3000mg per week! But that is definitely steroid abuse. As always, monitor as best you can. There are consistent suggestions that monitoring estrogen/ estradiol can be useful. My doc said probably not necessary unless you are showing symptoms like tender and growing man-boobs. However high T affects estrogen balance in males and there is a lot of info suggesting estrogen has a role to play in PC. It is great that you have medicos willing to look outside the box. I see supra-T as basically a management tool. Best of luck!
Re: continuous supra-T. The paper by Mohammad et al I referred to in the first post has a short discussion of this towards the end (p14-15,"Future Directions"). Very interesting. I did try it for 2 weeks but saw no benefit to me but no adverse effects either. There have been no systematic trials but there is a bit of anecdotal evidence. According to Mohammad its usefulness will depend on the individual pathway that T acts on the PCa cell in each case. Some pathways act on the adaptive mechanism, some on double strand DNA breaks. Generally they thought it has promise.
The authors of the Denmeade study explicitly noted that the use of Enzalutamide was responsible for most of the toxicities, and suggested it could be removed.
The chemo agent was etoposide, an old and little used agent. The reason was that it was known to prevent double strand DNA breaks from repairing and testosterone is known in vitro to cause double strand breaks. Denmeade et al concluded it was the cause of the toxicities they observed but said future trials should look at more benign PARP inhibitors. There seems to be a lot of interest in PARP inhibitors now and there are a number of trials happening using modern PARP inhibitors alone. I have been using niacinamide as a supplement as it is a known PARP inhibitor that is readily available over the counter. However it is weak compared to the latest molecules from big pharma. There are too many variables for me to say niacinamide has an effect but I suspect it is minor.
Just saw your post ; didn’t come up at first for some reason. Yes, the AR-V7 impact on Supra T was part of what my dr was talking about. Since I am in this Supra T range by chance ( related to Xtandi I understand), I am trying to get as much info regarding it as possible.
The most fascinating Post and replies ever! Who needs Audible. Don’t worry. All we like sheep will not follow--other than to read. You are one brave soul, kaptank. Mrs. S
Somehow from all these posts I feel like I just reviewed the 4 page documentation that's included with all of my medications. ??? WTF it's all Greek to me... and I'm Greek.
I was interested in the BAT effects before I had bone mets big enough to show up in PsMa gallium scans. Dr Sam Denmeade conducted trials of BAT at John Hopkins Hospital in Baltimore, and funded by US army, so I guess there are a lot of old soldiers with Pca, an a cheapfix was sought for them.
The idea is that while castrated using Zoladex, Lupron, Lucrin etc, and when Psa just begins to rise, adding monthly 400mg short of testo might overload intake of testo to Pca cells which grow more receptors for testo to increases the amount of testos getting into Pca cells, like a fisherman who hangs 2 rods and hooks over side of boat instead of just one rod and hook to catch more fish when there are not many fish around.
I have never seen any of the John Hopkins trial results.
But all sorts of claims were made prior to this time in 2016. Some had initial Psa flare, thenbig reduction of Psa and after whatws thought to be a standard of 4 montly cycles the Psa was lower, and it was thought the Pca was made more sensitive to ADT drugs, because the ones with high number of testo receptors were killed by testo overdose, leaving cells which were still sensitive.
Not all men responded, a few got very goodresponse,some got none, and anyone with bone pain from bone mets got higher bone pain. So when my bone mets showed up in scans I decided I'd be a fool to try BAT, and sure, testosterone is available online because body builders and cheating sportsmen buy large amounts,and might use 800mg a week whichb causes balls to stop producing
natural testo, and to boost muscle growth the total higher amount is maybe twice normal levels. Men from19 to 45 use testo mainly and IMHO,they would very much boost their chances of getting Pca.
So, no BAT for me, and I'llfind out later today if Docetaxel has had any Psa reduction effect on my bone mets, and justv what my Pca status is after yesterdays scans which cost a total of about $1,000, with Medicare funding $300 of the total, afaik. I think I need Lu177 or Ra223, not BAT. I'll know confirm what's going to happen with treatment options later today when I talk to onco doc and have 5th chemo inject at 1:30pm.
Hi Patrick, the paper by Mohammad et al I referenced in my first post has summaries of the Johns Hopkins results. They limited it to men with no pain symptoms. Its wise not to consider T while doing docetaxal. Best luck to us both!
Well, I'll read report, I ain't up to date with latest on BAT.
Yes, I agree about having testo shots during Docetaxel = no good.
Today the oncologist says there was uncertainty in my status of Pca because CT scans showed some new bone mets compared to previous mets.
BUT, Psa has gone down from 45 some 8 days ago to 26 yesterday, and that bodes well when I previous thought Docetaxel was no good at all.
I hope the rate of Psa reduction lasts a good long time.
BUT, future CT scans may show no reduction in size of bone mets because a dead bone with vastly smaller Pca activity that is not increasing will still show up in CT scans. The size would increase with increased Pca in mets. In my case, PsMa scan shows activity there, and other places but only enough overall to give a fairly low Psa of 26, not a terrible situation where Psa is 260 or 2,600, which it could be.
I sit each day upon what I call Puff the Magic Prostate Grenade, and it has been trying for years to explode ungraciously, and the mutated cells that have exploded to mets have in some ways become a clumsy but lethal large Rotweiler dog, and chemo is like a small agile fox terrier dog that dives between the legs of the big cancer dog and bites it on its legs, as well as on its dangling balls and this is killing the big nasty dog slowly, bite by little bite. It may not be expected to kill all the big dog, which has the unfortunate property of slow and lethal re-generation, even where chemo has nearly killed all of the dog.
The PsMa scans showed my mets generate Psa and are thus PsMa avid and that Lutetium 177 or Radium 223 would be a good fix.
Basically, the Lu1677 is like having a really nasty Aunty Lutetia wander around the body in blood stream but when she finds the door open at a Pca she invades, and ruins the sadistic fun being had by Mr Cancer, and of course his reaction to this is to mainly die, but while he dies, he says "I hope ya didn't bring Unkel Radium with you as well did ya?"
Usually when such unwanted guests arrive to intervene in a wild party that's out of control, its not unusual for some collateral damage to healthy cells which the body has trouble to dispose of. Also, Aunty L also likes to drop into Saliva Glands, a nice guy who wets your mouth with wondrous liquid full of goodies that have fabulous teeth and mouth cell preservation effects.
So Mr S Gland can be killed, so one guy I know who has had 7 infusions with Lu177 chews on frozen pieces pineaple which are cheap, many are grown in Queensland. Another lost his Mr S Gland after IMRT which is Xrays for a small tumor in his neck, which then vanished, and before his Pca which seems to have gone after RP and with EBRT some 5 years later, and all without ADT.
So he uses a cetain brand of chewing gum or else his mouth dries up badly, and the ordinary chewing gum just makes a horrid sticky mess in his mouth..... Oh, the joys of side effects! But all better than being dead.
I tried to read the content of the link you supplied but it was extremely difficult to understand and I wanted to see what Dr Sam R Denmeade had to say because he was in charge of US army funded trial of BAT at John Hopkins hospital in Baltimore. More Googling produced this report written by Dr Denmeade :-
He says the BAT gives benefit of more time to many castrate resistance Pca patients who are asymptomatic and where enzalutamide has failed, and that after BAT has completed in 4 months the Pca sensitivity to enzalutamide increases, so Psa suppression with enzalutamide can be repeated. This all adds up to increased time on Planet Earth. But I would not attempt DIY BAT because I have bone mets and you can get severe bone pain with BAT where bone mets are present. I'd say if I did BAT now, it would be like throwing a can of petrol on a fire.
BTW, I had time to read my radiologist report of latest PsMa Ga68 scan for 20/10/18 compared to previous PsMa Ga68 scan last May, which was about 2 months before chemo start in early July.
There is now no Pca seen in lymph nodes, and a long list of soft tissue organs have no PsMa uptake. It means Pca in soft tissue has reduced to below detectability threshold, or else whatever is there that has no PsMa avidity.
The PsMa scan shows more bone mets and larger mets than seen in May, but I think most increase in met size was due to absense of anything to stop its growth between the time Zytiga failed and beginning of chemo.
Before I said my Psa has nearly halved from 45 to 26, but pathology report said Psa was 36, so my onco told me wrong figure, or I did not hear clearly what he said.
But a Psa drop from 45 to 36 in seven days, 1 week, is a rate of 45 in 5 weeks, and the halving rate of Psa reduction could be roughly 23 in 2.5 weeks. So the sequence of possible Psa results could be from 36 now to 19, 9, 4, 2 over
next 12 weeks.
The likelyhood of this happening is equal to possibility of development of porcine flights due to genetically varied pigs
At least I see a Psa reduction, and just what now happens over next 3 months is anyone's guess, and my attempt at predictive mathematics may be complete fake info, aka BULLSHIT, but its always nice to explore possible outcomes.
If I end up with Psa of 1 after a full 10 cycles of chemo, 30 weeks in fact, then the Pca may resume its activity of growing, and the doubling rate would soon return to a high rate and evidence of this is seen in many cases and the Psa soon goes to where it was at chemo start, and a man is back to square one.
This can be dangerous if the increase in Pca is due to mutated forms of Pca which does not respond to taxane based chemos or to any RT.
But I have not included the effects of having Lu177 with maybe Ra223 as well, and my onco suggests I see Dr Lenzo for Lu177 during 6 weeks. If Lu177 did not occur, at least I could have expert opinion on what's best from Dr Lenzo who appears to be extremely well educated about the future possible success of his therapies because that's all he does, and the govt keeps an eye on him.
At least the combined chemo and Lu177 seems to be therapy that may give me more time on Earth than anything else anyone can think of.
Yes, I think if I were in your place I'd be looking at chemo and Lu177 too. My aim is to manage the cancer until I die of something else (preferably old age)
Did not think I would ever detail my brief experience with a version of BAT, but here goes.
After Dr. Snuffy Myers retired, he referred me to a well known Med Onc in New Orleans. At our first and only meeting, he put me on a "treatment" of daily rubbing my upper arms and shoulders with AndroGel, a testosterone replacement product. At the time I had run through all available drugs including Lynparza, a PARP inhibitor, and proton beam radiation, since DX in 2012 with Stage 4, many lymph node mets. At time of this one-off trial, PSA was 4.8 and had been rapidly rising. I, and this world class Med Oncs nurses thought, chemo was my next step.
Back to my AndroGel treatment. Goal was to get T to 1000, quite a jump after 5 years of continuous ADT to keep it down around 5! As you might guess from this cautionary tale, as T rose, never getting to1000, PSA took off, getting to 18.5, after several months of applying more and more daily pumps of AndroGel to body. After stopping the AndroGel applications, T dropped, as did PSA, but PSA did not drop back to pre AndroGel "treatment" level.
As next step now had to be chemo, had Axumin scan, which picked up some hot lymph nodes PLUS worrisome activity in liver.
Next was MRI of liver, which confirmed 20+ lesions in liver and CT guided biopsy of liver which confirmed PCa in liver.
Prognosis was 1 year with treatment, so immediately began chemo with Docetaxel/Carboplatin combo managed by my Atlanta Med Onc. After 6 cycles, PSA dropped from 10.8 to .4 and liver lesions less distinct.
So, did the failed attempt to run up
T with AndroGel (which ran up PSA), encourage PCa mets to set up home in my liver, where they had never been? We will never know, but I have my personal opinion.
I think all evidence so far indicates that testosterone replacement therapy (gels, patches etc) do not get you to genuine supra-T and the danger is that the T levels might be low enough to encourage the cancer. The only way I know of is intramuscular injection to give a sudden spike. I was aiming for T levels about twice the normal highest level.
Today, in The States, obtaining Testosterone Cypionate in "The Grey market" is somewhat difficult as it's a controlled medication..I suppose it can be done but it's tricky and difficult..
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