Very interesting article. Prostate ca... - Advanced Prostate...
Very interesting article. Prostate cancer 'cured' by shocking prostate cancer with testosterone.
Hi Paulofaus: Curious stuff alright when testosterone amped up "cures" one man's PC. Goes contrary to the orthodox thinking out there. U know that when U have met one man with PC, U have met one man with PC. No one size fits all. I can entertain the notion in some, few, select men, that the reverse thinking is possible, that additional doses of Test. could have the paradoxical effect of eliminating the cancer. That is why the precision medicine initiative movement included in Biden's Moonshot efforts need to identify the unique characteristics of our own PC, and then prescribe the individual treatment plan to that man based upon his genetics, his type of PC, and the progression thereof. I know several men who had successful treatment for PC, the first time around, who are now hounding their Urologists and Medical Oncologist's for taking testosterone supplements. Key is to figure out the patient and what his personal treatments needs are. We are heading that way with the PMI movement, precision medicine initiative. Docrok
Very interesting- pray everyone with prostate cancer will be able to use it someday
Very interesting article. I do have several questions. How many in the study? How many experienced a positive effect? What were the prior treatments? Were they also taking medications or had they stopped? What was the requirements for study entry, PSA, Gleason score, involvement, any indication of metastasis, etc.?
I agree. there 7s no link to the actual study or where the information can be found
The article is a bit misleading, I feel. BAT is castration therapy, where testosterone [T] is introduced periodically, in order to prevent the cancer from becoming resistant to castration.
Most men will fail ADT within 18-24 months. BAT is a way of prolonging ADT effectiveness.
Basically, unlike intermittent ADT (IADT), where the on-phase might be 12 months and significant survival mutations might have occurred, BAT involves frequent T injections, in an attempt to reset the clock.
Unlike IADT, where the off-phase may improve QOL, BAT uses T only for a short period in each cycle (one injection).
Odd that all of the British papers have these Johns Hopkins study findings (presented in Germany).
Too bad they all have "cure" in their headlines - based on one man in the study group (46 were not cured). Sets unreasonable expectations.
-Patrick.
Do I have this clear. instead of cycling on and off adt which may allow pca to run amok , BAT therapy interrupts therapy with a testosterone injection in order to reduce the probability of castrate dependent disease? obviously different oncologists, have their own principles but according to your research has one proven more effective and is there any way of predetermining which patients are better with straight adt, BAT, or interval adt? does interval adt help in anything but QOL , meaning is a man less likely to become castrate resistant by stopping and starting adt? thanks for the wealth of information you always provide. it has been very helpful in allowing my father to know there are treatments that have not been explained to him by his oncologist
PCa adapts to a low androgen environment by becoming super-sensitive to androgen. Over 20 years ago, someone (I forget who) hypothesized that, just as ADT kills many cells but selects for resistant cells, the reintroduction of testosterone would kill many resistant cells and select for cells that were basically identical to the original cells.
His idea was that one could cycle indefinitely. It wouldn't be a cure, but it could last much longer than ADT.
I have thought about this a lot, in terms of timing. Should one cycle rapidly? Every 6 months? A year?
The current BAT approach starts after 6 months of ADT, & then cycles on a 3-month basis.
When I am using T, I inject 200 mg testosterone cypionate weekly. With BAT, 400 mg is injected monthly (days 1, 29 & 57). During the 3 months of T, ADT is continued. i.e. the patient produces no additional T. I do not consider the BAT T dose to be high. Monthly injections might be a matter of convenience. It is injected into muscle & it hangs around a while.
BAT is experimental. So ADT currently only comes in two sizes: continuous & intermittent [IADT]. I believe that the times to CRPC are similar.
-Patrick
Hello Patrick,
I have a question. To the best of your knowledge does the low-T/high-T cycling work for early treatment of patients? Or is it only appropriate for patients who have long experience of ADT and have developed very high sensitivity to very small amounts of T - thus getting a bigger shock from the high-T phase?
I have a friend who failed primary treatment, has a rapid PSA doubling time, but has avoided ADT. He's hoping a high-T treatment will work for him.
Hi Alan,
When my RP was ineffective 12 years ago, & salvage radiation made no difference, I was faced with a low PSA but a short PSADT. There were not a lot of options then.
I had some androstenedione (a T precursor) & chrysin (to prevent the T converting to E2), & I finally worked up the nerve to try it. My PSA became stable.
Before my RP, there had been an abrupt end to nocturnal erections. Oddly, PCa can lower T production (ref. Patrick Walsh). I knew my T must be low (& E2 probably high).
So I did andro continuously for a couple of years. When the andro was running out, I found a doctor who prescribed AndroDerm. He also gave me Arimidex (he was wary of chrysin).
& that was fine for another 3+ years.
Until it wasn't. I then began knocking the cancer down (3 months) & swiching back to T (3 months).
For your friend, I would suggest that he gets his T & E2 (estradiol) tested. If T is normal-high, I don't see how additional T will help him.
If T is low, it would be interesting to see if TRT has a beneficial effect on PSADT. If very low, I'd expect to see some change.
Regarding E2, which should be 20-30 pg/mL, it is my belief that estrogen dominance spurs growth. E2 cannot affect growth when T is at castrate levels, but when T=300, say, & E2=40, T is growth-permissive. At normal-high T, E2 can be resisted.
Doctors who traditionally treated hypogonadism, typically aim at getting T above the cutoff. I have always aimed for normal-high. Usually, I am around 1,000 ng/dL. I sometimes see references to 'very high' T being used, but actual patient numbers achieved don't look super-high to me. I don't see why one would aim above the normal range.
My RP, according to Walsh, would have restored some T production. At one point, I figured that the AndroDerm patch was maybe giving me a little over half of the 1,000 ng/dL, but who knows? The point being that the ideal dose will vary with the person.
With a patch, treatment can be stopped quickly should the PSADT shorten. Injections take longer to clear.
So far, I have been writing about the restoration of normal T functionality. For the "shock" aspect, I'll refer you to the BAT protocol, which begins with 6 months of ADT.
However, I would start with 3 months & get a PSA test. If it is very low, begin the T phase. If there is a feeling that the PSA could go lower, consider another month or two.
My idea here is that you want to get optimal benefit from the ADT phase before switching to the shock phase.
...
I have dealth with more mundane issues in my posts, that might not excite much interest, but I'll mention two. While he is getting T & E2 tested, also test:
1] CRP & albumin. Controlling inflammation can improve the PSADT.
2] D-Dimer & fibrinogen. Controlling coagulation dysfunction can lower the risk for metastases.
I'd be happy to comment on the lab results.
-Patrick
Thanks Patrick, that is excellent information from a guy who has both studied the problem and had personal experience.
I'll pass along a link to this thread to my friend.
Thanks again.
My husband’s psa was always low at 1.25, even with Gleason 9, stage 3b at diagnosis. Pathology confirmed NOT neuroendocrine. Since RP in 2018, he’s had salvage radiation to prostate bed along with 6 month lupron in 2018, then sbrt and cryo to the inferior pubic ramus a few months ago (highest psa 0.48 on bone recurrence). Cleveland Clinic, Mayo, MD Anderson all consulted.
What is interesting to me is his t was always high normal, but he also was in the young side at diagnosis (52). His bone lesion recurrence did show on axumen, psma, and choline scans with the super low psa. The psa was only nondetectable during the adt and for 9 months afterwards.
Seems we are getting differing opinions of how to proceed from the three well known institutions, which is so challenging. More scans in May but I want to have a better idea of how to proceed if there are more metastasis. Currently not on adt.
Dr Leibowitz uses high testosterone on certain patients. Here's his spiel-
There were only 16 patients in the trial and what the article fails to mention is the trial involved "etoposide" which induces "Top2" double strand breaks along with 400mg testosterone injections. This apparently cripples the tumor cell's DNA repair mechanism and leads to apoptosis.
the etoposide has been abandoned as unhelpful, and making people too sick.
Interesting, but not exactly news.
Good study, in that it is part of an attempt to figure out the role of testosterone in prostate cancer, beyond saying it is "fuel".
Reading the comments below the article, I am somewhat confused. what has scientifically been clearly established? does testosterone or metabolites of T feed prostate cancer? I understand the shock method, but the comments below the article call into question whether high estrogen and low testosterone "cause" pca to proliferate. if anyone has a more clear answer to this or articles that argue both sides please share.
There certainly is an involvement of testosterone, a sex hormone, in the prostate, a sex gland. And clearly reduction of testosterone can bring prostate cancer to a halt for a time. That has been demonstrated for 50 years. Beyond that, it seems to get a little vague. Would testosterone supplementation have worked as well had it been tried 50 years ago? Was it changing the level of testosterone that made a difference?
Does testosterone "feed" cancer as in "feed a fire", meaning make it flare up? Apparently, not always. "It depends". On what? To be determined.
It may be (and I think it is) that variations in the level of testosterone in the prostate gland exert a selective pressure on the prostate cells, which "try" to achieve a set concentration of testosterone in their cytoplasm (or is it in their cell nucleus?). The structure of the cells in the different areas of the prostate gland, with different testosterone concentrations, start to drift apart as to the count of androgen receptors, just like birds on separate islands in the pacific exhibit body "drift", which may or may not be due to a genetic mutation. (That is, you can get fat without there being a genetic mutation.) Then if cells that are "used to" lower testosterone get exposed to higher levels, they crank up, and create more PSA, but more relevantly, they replicate more frequently. That gives rise to BPH. But if the mechanism that limits cell reproduction is damaged, you get prostate cancer.
(speculation)
So I think that the testosterone level does not cause cancer, but within limits, can change the rate of metabolism of prostate cells, including prostate cancer cells, including the cell division rate.
That serves to make much more sense to me . thank you. I have an estrogen dependent disease, endometriosis , which somehow falls into similar oddities. I just needed to understand if pca is a testosterine dependent disease , and it appears that is not a clear cut case. thanks . that helps. I understand hormone depletion as I've been on Lupron and others to stop E production and shrink lesions, but I'm still learning what it's like for each man on Lupron emotionally. As a woman On Lupron I had severe migrsines, a mini strike because the doctor gave no estrogen back which she should have, and my bones ached so badly, not my muscles and joints from further disease but my actual bones , and of course depression and hot flashes . I was horrified when I knew my dad had to go in it because my own experience was so bad, but it seems men take well to it. my goal is to obviously research , but also to understand men's experiences as well as a woman can. ty for helping me as I hope to be able to help others someday. xoxo
i ran this study past our oncologist who firmly and adamantly said ''no way''. he said too many men in the study went on to show aggressive mets in the lower spine.
the article says : "because cancer uses it as a fuel".
Shows you the power of bad ideas. It's like gasoline? gak.
It is a sixty year old idea whose usefulness has come and gone.
the trials attempt to not be russian roulette
Testosterone Levels and Prostate Cancer Risk - 1
Testosterone Therapy in Men with Advanced Prostate Cancer / June 2019
man with prostate cancer
live with prostate cancer 
Osteoporosis with prostate cancer 
