I have tried to report my experiences with Bipolar Androgen Therapy (BAT). You will find them in my profile.
This will be the last as the anti androgen I use (bicalutamide) failed in spectacular fashion. I will post on subsequent treatments. The pattern of failure may interest. Hist: Failure of long running ADT (zoladex) was about 2015 when I started bicaulutamide. It failed after 12 months and I decided that was a good time to see what my reaction to BAT might be. All experiences differ but all information is potentially useful. If you have a doc who will prescribe it, then it is a very simple intramuscular injection once a month. You can easily learn to do it yourself (google it).
Stop bical a month before, continue ADT. Inject monthly until failure. BAT reduced PSA by 50% in a few months, plateaued for a while and failed at 8-9 months at PSA 5-6. Rechallenge with bical caused a quick 80% PSA drop, bit of a bounce, then plateaued at 1-2, failed after 12 months. OK I guess, an extension of a year on bical. Then I asked can I do it again? Each subsequent cycle of BAT got shorter and shorter but over 3 more repetitions it started to look iffy with PSA jumping around like a sockful of frogs. All up, BAT extended the use of bical for 3 years after failure at 12 months. A rapid PSA rise above my limit, 5 drew the conclusion that it had all failed and I saw my onc who advised a PSMA scan and continue bical alone.
The next PSA declined to about its previous OK level and the scan showed against the scan I did about 4 years ago that there had been little growth in that time, 2 old lesions had started to heal and 2 extra lymph nodes and a spot on a rib. Oligometastatic. Had my conclusion been a false positive? I did stereotactic radiation on all mets and continued bical alone. On one month (about the 10th) I tried a single BAT. PSA screamed up, a new PSMA just 12 months after the previous showed significant growth. Now 8 lymph nodes and 3 bone. More growth in 1 year than the previous 19.
Now I am certain the BAT did not cause it. That much growth in 1 month is impossible, it had to be growing throughout that year. When bical fails it changes its action and promotes cancer growth. Most likely thing I think is that my original conclusion of failure was pretty close to the money and that a gradually rising trend was masked by the PSA drop caused by the radiation. Anyways, there’s a lesson there. Watch closely for failure on bical.
My other big mistake was probably continuing each type of treatment (BAT and bic) to their respective failures. (and also not starting earlier) An alternative sequence is bical 3 months, nothing for a month, then BAT for 3 months. Then, in 2nd week after3rd shot, start bical again for 3 months, month off, BAT for 3 months. Rinse. Repeat. Well, something like that. Patrick will have useful things to say.
I went on to abiraterone(abi) (plus of course prednisone). I am now in an interesting trial of abi plus the PARP inhibitor Niraparib. I will separately report on my experiences there.
OK, so what can we say about this treatment? Firstly it’s a very simple management technique to reverse/reset/prevent resistance to anti-androgens/lutamides. (it works well on enzalutamide too but doesn’t work well on abi). Fairly safe but good medical advice advised. In particular, If there is bone pain then you may have a torrid time. The pain is likely inflammation rather than growth of the cancer per se. You will know in 3 months whether it works for you. It is important to bear in mind that it is a secondary treatment, not a primary. Primary treatment is ADT+anti-androgen. Experiences may differ. I have not commented on continuous testosterone therapies.
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I'm doing continuous testosterone.Estrogen patches for ADT for a 6 month leadin and for the last 17 months high testosterone.
I'm doing well so far but am researching and thinking about what to do next. Perhaps Deca cycled with Cypionate? Or DHT blockers cycled with DHT floating,?
At the time bical had a tick by our medicare system but the really expensive enza could only be dispensed after bical failure. These days someone at my stage then would probably start off with abi.
Thanks for posting. Perhaps the most important takeaway (at least for me) is that it is indeed possible to return to bicalutamide after initial and even repeated failure and still get some mileage out of it. (Dr, Bob Liebowitz claimed that was NOT possible, and that once it failed it would ALWAYS act as an AR agonist and feed PC progression.)
Yes.. Bicalutamide failure CAN be reversed. Interestingly, some researchers are trying to make bicalutamide salts like Sulfites, sulfones etc. which can potentially work again even after initial failure of regular bicalutamide.Its too early for me to confirm results of my Bicalutamide monotherapy which I am doing intermittently.
On Jan01, I stopped ALL meds....PSA was 0.3 and ALP was 49. PSA rose to 3.6 and ALP to 69 in 6 weeks. Restarted Bicalutamide 50 mg/day with Dutasteride 0.5 mg /day and today (after 2 weeks) , PSA came back 1.5 and ALP 59. So the plan seems to be working so far. My low set point is 0.3 and high set point is 3.5.
I suspect suforaphanes have something to do with prolonged effectiveness of Bical. I eat a lot of Sulforaphane rich foods daily. A deworming med. Niclosamide in under research for reversing bicalutamide failure.
For people who question efficacy of Bicalutamide, I would like to say " Bicalutamide works beautifully and has the least side effects of all PCa meds..so it should be used until it truly fails.
My total ALP fluctuates between 45 and 70. My Bone ALP was 10.4 about 3 months ago. I get BALP every 3 to 4 months. Its due in March.
For me its crucial to watch markers closely as I am experimenting against advice of SOC and my Doctors. Will jump back on lupron train if I see any cracks in my plan.
The fact to keep in mind is that degree of aggressiveness is paramount feature when it comes to PCa treatment. That's why different men react differently to the same treatment. Aggressivity depends on genetics, gleason grade, type of variant ,comorbidities and other such factors. No two men have same PCa.I can not prove it scientifically but I think that our physiological state and general health is lot to do with how we will respond to a given treatment. Lack of testosterone in a man is a totally abnormal physiological state and therefore it can cause difficulties with our immune system and overall cancer fighting capacity. When we allow T to come back up, we are pushing our body back towards normal physiological state. But, its a risky venture as T can sometimes promote cancer cell growth. The role of certain foods is also valuable in how we respond to treatments. Foods rich in Sulforaphanes, Resvesterol, Lycopene, Quercetin ,EGCG (tea) etc. tend to keep treatments working better. One should eat a lot of such anti cancer foods every day. And Physical exercise and improved blood circulation caused by constant body movements does help. Then good sleep and less stress might be other beneficial factors.
All this is my speculation ...do not ask me for randomized clinical trials as I have none to prove these .
Using high dose T for BAT theoretically could cause enough feedback inhibition of endogenous testosterone so that testosterone levels could drop to very low levels, even castrate in the final two weeks of a BAT cycle without ADT. Only way to know would be to test T levels during that time.
Good question and answer is unknown. Using high dose T for BAT theoretically could cause enough feedback inhibition of endogenous testosterone so that testosterone levels could drop to very low levels, even castrate in the final two weeks of a BAT cycle without ADT. Only way to know would be to test T levels during that time.
BATMAN data shows that 2 weeks after a 400 mg shot of T cypionate the exogenous testosterone is cleared and quickly goes to zero. So a test at 3Weeks will show him well endogenous T is being suppressed on the absence of other ADT. Yes?
The length of the high testosterone will depend on how you conduct BAT. Cypionate will drop from 1600 to <20 in 5 weeks if no more injections are made. There are shorter half-life forms of testosterone. Also T patches. I don't know if T patches or gels will get your T up high enough though. Perhaps combined with a lower dose of Cyp. So then it would go down faster.
A few hours after I inject my T is over the lab measurement limit of 3000 and before I inject the following week it's dropped to 2100. I'm doing continuous high T after a 6 month low T lead-in so I never let it go lower than 2100.
WARNING. There are indeed shorter half life forms of T. One used by body builders is testosterone propianate. NEVER USE IT. It causes a pain in the thigh not unlike an accurate rear leg strike by an enraged bull. Guess how I know. It is painful even in small doses. The body builders use it to quickly pad up muscles and say just be a man.
All my medical advisors agreed that extending the use of bical (despite more powerful agents being available) was a good thing because bical is cheap, doesn't create resistance to the more powerful agents, and is benign in terms of side effects.
I'm interested in your bicalutamide cycling and results.
You mentioned 2 me recently to go the route of bica / monotherapy after my recent BCR posting.
My PHONE was with my R O who was acting as an \M O as well - it turns out, he won't be managing me any longer IF my upcoming referral to the 'M O' team of specialists at the cancer center allows THEM to prescribe Bicaluamide, which is not the SOC in Canada.
IN other words - I 'graduate' from under his wing - he doesn't DO advanced 'chemo' and MOST patients who go beyond the basic SOCs (radiation and ADT) are above his pay grade. I was surprised to hear that, but he said he would prescribe it IF they turned me down - something I deeply appreciate without knowing what the result(s) might be over timelines. Apparently he had some experiences with that in Scotland - but he insists it must the 'old' U K ' dosage of 150 mg daily. There was no mention of any other 'stuff' to accompany 'Bica' - so I guess monitoring is the game plan.
The MAIN reason I have a visit set up for the 'MO" team ? - I requested chemo - in fact 6 infusions of Docetaxel - to try to KILL the spread of castrate sensitive cells in my lymphatic system.
Perhaps I am full of 's$!t' but I wonder if a 'cure' is still on the table for me - After Dx of about 3 1/2 years, my recent BCR and PSMA shows local / regional spread only and wonder if a knock out punch is still possible.
I will 'confront' them with a question - are we waiting for a long(er) / short(er) terms growth and morphing with the standard of care BEFORE you intervene TOO late with systemic chemo OR why not try ot get it before time allows it to overrun the body ?
Another question will be - can enough time elapse on Casodex / mono to KILL off the cancer cells and put me into remission THAT way - thinking about 2 - 2 1/2 years ?
I'm in no position to dictate, but is the SOC a recipe for failure ?
Can I ask you what the Dutasteride component of the monotherapy accomplishes ?
And the comment about the de-wormer - I've read something about that before as well - perhaps from U ?
As usual, I appreciate your input(s) .... and why you would cycle I'm being lazy here, but the 'progression' in your case would have you on a lifetime of ADT and the mono is more tolerable for all kinds of reasons.
I am doing an experiment. I have assessed and concluded with extensive lab tests and biomarkers that my PCa comes into "dove" category.. meaning it is not very aggressive. Further, I could achieve a very low Nadir PSA (less than 0.2) in first 12 months of ADT. Another positive sign. General health is pretty normal. Based on all the facts, I ventured into Intermittent ADT adventure. Side effects were also motivating factor.
I believe the researchers who say that continuous ,strong suppression of Testosterone does cause faster androgen resistance and worse Neuro endocrine changes. My hypothesis is that if we use ADT off and On, it keeps the effect long lasting and that Bica is less likely to fail sooner.
Note that because it is an experiment, I monitor labs very closely , (every 2 weeks) as it entails risk trying such method. My last Injection was 15 months ago and so far Bica is doing its job and I am happy with my quality of life. Its still early as this month I will complete 2 years since my diagnosis. Its not possible for me to give any advice without knowing all details and test results of an individual person.
When I was diagnosed in 2004, there wasn't much happening in the PCa drug world. Lupron had been FDA-approved in 1985. Bicalutamide (Casodex) had been FDA-approved in 1995 at 50 mg/day in combination with a GnRH analogue. [The FDA declined to approve the 150 mg monotherapy dose used elsewhere.] Docetaxel (Taxotere) was about to be approved for metastatic CRPC (then called androgen-independent (hormone-refractory) PCa. It was seven years before Abiraterone was approved. Thinks looked bleak.
But I had read a crazy hypothesis from 10 years earlier suggesting that testosterone [T] might be used to resensitize PCa to ADT. As it happened, I was in a window of opportunity for legally buying androstendione, a T precursor. Within 9 months, possession would be a federal crime.
The BAT papers started to appear in 2010. In the meantime, I was in my own n=1 study.
From Australia, there had been an editorial: "Testosterone Therapy in Castrate-Resistant Prostate Cancer: A Possible New Approach" in 2009 [1]. (Christopher Sweeney is now at Dana Farber.)
I had in my back pocket the idea that diethylstilbestrol [DES] might be useful if/when I progressed to CRPC. In the U.S., Eli Lilly stopped making it in 1997, but some compounding pharmacies can supply it.
There was an early Japanese study that used DES for CRPC. In 2011 there was a Chinese paper: "Clinical study of diethylstilbestrol in hormone refractory prostate cancer" [2].
"When used for the treatment of hormone refractory prostate cancer, diethylstilbestrol at a daily dose of 2 mg can achieve a PSA response in 27.5% patients and a PSA stability in 24.1% patients. And the median time to progression is 4 months."
"DES has at least three mechanisms of action in the treatment of prostate cancer in men. It suppresses gonadal androgen production and hence circulating androgen levels due to its antigonadotropic effects; it stimulates hepatic sex hormone-binding globulin (SHBG) production, thereby increasing circulating levels of SHBG and decreasing the free fraction of testosterone and dihydrotestosterone (DHT) in the circulation; and it may have direct cytotoxic effects in the testes and prostate gland." [3]
For various reasons I decided to make DES part of my BAT protocol in 2018, rather than continuous Lupron.
If a quarter of CRPC cases see a PSA response, I wonder if 2 months, say, of DES might reverse resistance to one or more androgen receptor axis therapies, or BAT? Clutching at straws perhaps, but I do believe that DES does things that high-dose estradiol patches do not.
Thanks Patrick. I was diagnosed in 2002 and I remember the shortage of useable options. DES was not on the radar then of my medical advisors. Any thought of testosterone in any form was literally heresy. We have gone a ways but still don't really know who is likely to benefit, with robust large scale trials unlikely for obvious reasons. Anecdotal knowledge is better than no knowledge so reporting our own experiences here is well worthwhile. A data base is emerging but there are still many things we just don't know.
Thanks for your insights and experience. I’m actually starting today on my own first trial of modified BAT for HSPC. Will do testosterone cypionate 200 mg/wk for four weeks and then stop and follow PSA response with no ADT to see if I respond favorably or adversely. If the former, then I may do a one month cycle of T every 4 to 6 months to maintain some muscle mass and hopefully prevent emergence of castrate resistance.
Don't do PSA in first month. Completely unreliable and scary. I think (that's all it is) that you need to go 3 cycles at least to see what the effect is.
What was your psa at each step including at diagnosis plus what was your treatment after diagnosis? Will help me compare to my present situation. Thanks
400 mg. Intramuscular injection. T cypionate usually comes in 200mg/ml solution. It's what Denmeade and the Johns Hopkins people used and they justified it because the FDA says it's a safe dose. I experimented with higher doses but concluded that was a good dose (alright maybe 500mg) and going much above that made no difference. Do a T bloodtest when T is at its highest and adjust dose as required. Some need more, some less. You are aiming at a T level that is 2-3 times above the top of the normal range.
I read all about BAT years ago but when I began seeing bone mets in PsMa scans I knew that BAT would not work, and just cause pain. It is interesting that you say bicalutamide ( Cosadex ) acts to boost Pca growth after initially slowing down Pca growth. I watched a friend who had RP, then ADT then salvation RT to RP site and ADT lasted 3 months, and extra RT gave only a few months, then Cosadex boosted Psa from 7 to 40 in 3 months. Any form of anti hormone drug seemed to do SFA. So he had 10 doses of Docetaxel and over 7 months his Psa went from 40 to 2 after 2 doses, then back to 40. They examined his DNA, he was Brca1+2 positive so they tried PARP inhibitor, and Psa went to 432. Then new mets appeared in his liver, and he got so sick he could not have Lu177 as he wanted, so he soon died in Hospital aged 59. It was major disaster for his beautiful wife and 2 kids.
I think he should have stopped chemo soon as Psa began to rise, and then he had a chance to get Lu177. It may have stopped the spread to his liver. But nobody, including his doctors, could really understand enough or do enough.
After 4 doses of Docetaxel, my chemo was declared a failure, so I went to Lu177, Psa 25. $ doses + Xtandi got Psa to 0.32 in 1 year, not bad, but in 7 months, Psa was back to 30 after
Xtandi failed, so I had 2 more doses Lu177, and Psa went to 7 last November. But since then its gone to about 200 now and I have only bone mets. So I had my first Ra223 ( Zofigo ) 3 days ago and I have had no side effects yet, and I feel good, and still have no Pca symptoms.
If Ra223 kills new and remaining old bone mets which have very low PsMa expression then I might do real well. But I had to ask for the Lu177 and beg for the Ra223 before docs agreed that what I wanted would be OK and better than more chemo which was unlikely to work.
The idea is that if I kill bone mets which are not big enough to cause my bones to crumble, the damage to bone marrow will be kept to a minimum, and I'd have enough bone marrow left to live many more years. Many men leave it too late to challenge Pca in bones which destroys bone marrow, and by the time they do get Lu177 or Ra223, these things destroy additional bone marrow so they don't have enough, and Pca can continue, and they die of organ failure because bone marrow function is gone.
Lu177 was good to get rid of all my many mets in lymph nodes, but none in any organs.
It also zapped many bone mets, but after 6 doses, new bone mets appeared with low PsMa expression, so more Lu177 would have been a waste of time / money. So with all soft tissue or visceral mets gone, I qualified to get Ra223 which targets itself to Ca traffic at mets, and it does not depend on PsMa expression which varies quite a lot on some uncertain conditions that are not well understood by experts. I also suspect my continuing use of Xtandi could be boosting Psa rise. But other blood numbers don't indicate the same increase in bone destruction by Pca. I want docs to tell me why I need to continue Xtandi. But perhaps our Australian PBS scheme will stop them prescribing more "useless" Xtandi because Psa is going up. Our medical system does not allow Govt funded expensive cancer medicines to continue if its obvious they are just not working in any way to do that they are designed to do, or do anything else beneficial such as boost PsMa expression while having Lu177 doses.
Its a very day here folks. Radium went in OK, no side effects yet, and I spent 1.5 hours hard work clipping 1/2 my hedges. I'll swim a bit later this arvo.
Congratulations. That is quite a journey. It was wise not to do BAT with bone mets. Best of luck with the Ra. I agree that tackling bone mets early is important to QOL later.
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