Dr. Vogelzang uses high dose testosterone to kill PCa in advanced prostate cancer patients --search youtube "2020 Prostate Cancer DAY 2" for recent videos he says it causes double strand breaks / and floods the remaining cells making them unable to replicate etc etc really good stuff...
Dr. Vogelzang covers patient treatmen... - Advanced Prostate...
Dr. Vogelzang covers patient treatments for adv. PCa Uses high dose test. to kill PCa in nmCRPC / mCRPC search youtube for recent videos
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George71
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Dr. Vogelzang covers current treatments for high risk nmCRPC / mCRPC / mPCa
super high dose testosterone for cancer patients with active PCa --- talks favorably about CBD. search youtube "2020 Prostate Cancer DAY 2" for recent videos. He talks about treating mCRPC patients some for 20 years.
I looked through his slides. He does not mention high dose testosterone treatment in his slides.
he does in the video 9/12/2020
@ 1:53:00 in the video he begins talking about it.
In the video he talks about giving high dose testosterone to one mCRPC patient he has been treating for 20 years dropped his PSA from over2000 to 1200 in 4 months -- something like that.
Yes, after discussing CBD he gets to that. He mentions a study at Johns Hopkins, did they report anything yet?
I did not understand the name of the doctor he mentioned who tried high testosterone successfully in the past? Maybe he reported anything too.
Yes, Vogelzang said he is currently doing it to a mCRPC of his own -- he said he has been for 4 months -- reduced PSA nearly in half?? Dr. Denmeade does it bi-polar,
Dr. Bob Leibowitz, coutinuous SPT... below is a link to Dr. Denmeade's video
youtube.com/watch?v=6QFfntW...
here is Dr. Leibowitz
Here is a report about the study including 200 patients which Dr. Vogelsang mentioned:
BOYS:
LOTS of flack floating around on this treatment, in part as it goes against everything that is presently being done, but what the hell, shooting at stars sometimes hits.
WE need more data, more input and we need it fast to help our brothers, if in fact, IT DOES WORK. There is just such little real data to date-shocked to say the least, so it is up to us guys to do some digging and find out more, SO PLEASE, ALL OF YOU GET ON IT NOW,
speaking to your docs, researchers etc.anyone who can help us. TIME IS CRITICAL SO GET GOING TODAY AND GET BACK TO US ASAP.
IF THIS WORKS, we ALL need to support it and get on it, and I mean NOW!
Will do - speaking to dr Scholz about it in 4 weeks
excellent video about that --- with Dr. Schloz
go to youtube and search for
"How do You Treat Oligometastatic Prostate Cancer and What Does Cure Mean? | Ask a Prostate Expert"
We can post links to ASCO and anywhere else on here -- just not any from this source (copyright ??/ so don't post the link when you find it)
in reply to billyboy3
I've been on SPT for 12+ months. prostatecancer.health.blog/...
In 12/2018 I had RP. Two Mayo docs guaranteed me that cancer would return aggressively within 3 months. So far nothing. My SOC onc used to try to talk me out of my therapies but now tells me to keep doing what I'm doing because it's working.
History: prostatecancer.health.blog/...
Note that I've pretty much done 100% of all of these things without a doctor on board. I had to fire my Mayo docs because they were yelling at me when I told them I wanted to do estrogen patches instead of Lupron.
Probably what is working is my therapies. But I do have to entertain the possibility that I have just been very lucky so far.
billyboy3 in reply to
you need more time to assess whether this is going to work longterm. The biggest fear is it at some point superfeeds pc cells and you just blow up, losing perhaps years of life otherwise.
That said, you took a stand, not supported by anybody of experience in this arena, took lots of guts, I hope you are not wrong, for there is NO going back, if shit hits the fan. I had considered this at one point, but prefer going into battle knowing what is in my guns.
Please keep us update as often as possible, would suggest getting psa test monthly, and if things start to turn bad, to get back onto the usual without any delay.
Good luck Pal!!!!!
-FROM ALL OF US HERE!!!!!!
Also, make a detail list of what drugs you are taking, including make, dosage etc. and start a chart and get it to us as well.
thanks
in reply to billyboy3
Thanks! I have lots of backup plans.
History: prostatecancer.health.blog/...
Current therapies: prostatecancer.health.blog/...
Hormonal plan: prostatecancer.health.blog/...
When I see my doc in a couple of weeks, no more Lupron for me. Life with no T sucks. I was not designed for this. This is wildly exciting. If he says no T for me, I'll go to the VA for treatment.
in reply to ck722
I did ADT for 5 months. I hear you. No T sucked for me. I told my wife that 5 years with T beats 30 years with no T.
Yeah, not SOC, maybe doesn't work for everyone, but when the alternative is to be a girl? Give me the needle!
According to Dr. Morgantaler -- Higgins in his 1940's discovery / concluded that super low / testosterone kills cancer cells and slows progression and super high testosterone kills PCa cells and slows progression also -- he gave estrogen to shut off testosterone -- but few if any perused super high testosterone until about 30 years ago -- by then the false belief that testosterone was like pouring gasoline on a fire was already the mainstream belief being taught in med school to all doctors. Now they know the fact is -- PCa cells grow the fastest at very low and low normal testosterone levels... and hardly at all at castrate and super high levels -- only on super high testosterone you stay a lot healthier (no bone loss/ muscle wasting/dementia etc and on super high testosterone you can't become CRPC...
I have been researching this topic very actively recently, especially as how Supra-Phys T might impact my currently indolent (PSA<0.2) HSPC. Dr Leibowitz is certainly an enthusiastic advocate for long-term SPT to hold off castrate resistance. But the data is not there yet that demonstrates this with any clarity. Mostly anecdotes or very small series at best.
If you want to consider the mechanisms of action such as the induction of dsDNA breaks, cell-cycle arrest, AR mediated effects, etc., then one must consider the entire cellular and genomic biology and pathophysiology, not just pick one factor. Admittedly this is a complex system so there is no easy or clear answer.
The following review article covers this in some depth and provides (humbling) perspective with an investment of study:
mdpi.com/2072-6694/9/12/166...
As for myself, I am at a point of accepting that normal to high-normal T is probably beneficial to my physiology rather than my hypogonadal symptoms at T levels less than 100. And the bi-phasic model of T effects on PC suggest this is the worst place to be (rather than fully castrate or somewhat high T. Whether 300-500 (normal-ish) or SPT at >1500 is unanswered in my view. I will be considering for the future: possibly using infrequent pulsing of high T doses (perhaps once every 3 to 6 months) to shock any theoretically emerging CR cell sub-populations. But monitoring PSA response and being vigilant about scans will be important. There is risk in the uncertainty. I am not yet prepared to commit to this as a personal trial.
Please study and consider all evidence carefully before committing your precious life! How might supra-T impact your non-cancerous cellular systems affecting aging, senescence and other aspects of health?
The Mahommad article you cite is still by far the best review of the field of high dose T. A more recent review concluded it was time for phase 3 trials for BAT but there wasn't really much new data. What is now clear however is that supra T is relatively safe. There are a few conditions. Most trials are for asymptomatic patients. Continuous supra T requires very careful control of estrogens (body builders have shown that)
I advise anyone considering this to do a rigorous risk analysis. Discuss fully and frankly with your onc. They will disagree and try to talk you out of it. Consider what they say. The bottom line I laid down to my onc was that she was my advisor. Advisors should be listened to, but not necessarily obeyed. You need to do your own research. Your position and risk toleration is necessarily different to theirs. When I decided to go ahead against her advice it became clear she was not the sort of person accustomed to being disobeyed and we parted. My current onc knows and disapproves, but is willing to talk and suggest best SOC strategies. I think the best use of supra T therapies is to prevent, delay or reverse resistance to conventional SOC as it evolves. It is at its best in combination with other therapies (and not just those operating along the "androgen axis"). The evidence that it can be a primary stand-alone treatment is thin at best.
"How might supra-T impact your non-cancerous cellular systems affecting aging, senescence and other aspects of health? "
You will likely look like my son and a couple of his doctor friends -- or hulk Hogan or Schwarzenegger -- Franco Columbu -- Jack LaLanne and die at 97
Furthermore, from the same article is this consideration which gives the case that may favor continuous high dose or SPT verses pulse dosing such as BAT:
"The relative success of the modern studies employing the BAT approach are encouraging,
but the extent to which the clinical benefit observed in these studies reflects the bipolar dosing
strategy or the documented achievement of truly supra-physiological androgen levels remains unclear.
Preclinical studies have consistently found that SPT delivered on a continuous basis represses the
growth of PCa cells, and no studies (preclinical or clinical) have directly compared continuously
administered SPT with BAT. Whether rapid cycling of SPT (vs. continuous SPT) is necessary to achieve
the clinical benefit or delays resistance by preventing adaptive AR-downregulation remains to be
determined. Ultimately, the predominant mechanism of SPT action may dictate the ideal dosing
strategy, with continuous treatment likely providing improved efficacy if the main mechanism of SPT
action relates to changing from a “low-T” oncogenic AR transcriptome to that of a more differentiating
SPT transcriptome [97], and BAT demonstrating more activity if repeated cycles of DNA damage is
a critical mechanism of action. However, continuous SPT can repress the expression of genes that
repair DNA damage, and thus the continuous repression of these repair programs may also exceed the
responses seen with BAT."
You are right on it...
That is what Dr. Leibowitz says in this video -- 4 years ago.
That is right: we just don't know. In my experiment with BAT I did a couple of weeks of continuous supra T: 200ml every 2nd day. I didn't notice any significant difference to my reaction to BAT and finally wimped out back to BAT. What would longer term use do? I don't know but I would guess it would fail at some point, just as all treatments to our fiendishly adaptable critter fail. We have our best chances alternating supra T with no T.
I know leibowitz advocates continuous high T but not for everybody. We don't know his selection criteria. I was actually responding to your previous post quoting the Mahommad paper that the choice of continous vs BAT would depend on the predominant actual pathways in each individual case amongst the many possible pathways that high T can maybe act on the PCa cell.
I see -- I thought you were saying BAT was likely better than continuous SPT -- and his program shows a much better outcome than BAT
We don't know that. His evidence is anecdotal. At the moment the best and only "reliable" evidence is the various BAT trials associated with the Johns Hopkins group. There have been individual stories of hi T since before the 1980s but no systematic trials and really no good info on whether it was true supra T or just high physiological level T. They are all case studies and results vary and we cannot really compare them. So it is literally true: we don't know. Mahommad summarises some of them and the limitations are obvious. Fact is, we don't know a lot about continuous supra T in the presence of PCa. BAT is also in principle safer than continuous T simply because the exposure to supra T is much shorter for BAT.
Incidentally, don't think that case studies and good systematic studies are at odds. Every one of us is our own case study and from where we are, large number statistics are part of the background but in terms of our decision making, we are very much "learning as we go", a different kind of evidence valuation (technically Bayesian statistics). I decided to use BAT because I knew more about it. Continuous just looked too risky. I did try a couple of weeks of continuous supra T but ended up finding no good reason to continue in the circumstances. We are taking risks and it is our life at stake. Everyone thinking about it should post questions and comments because the more we discuss it the more we learn. Anyone doing it should post their experience so we can all learn. There is a lot of info already out there on this site. I see T therapies as adjuncts to conventional treatments rather than replacements: that is a "safe" way to proceed as we learn more.
in reply to kaptank
I've been on SPT for a little over a year. NED. PSA = 0.028.
My history: prostatecancer.health.blog/...
My current therapies and status: prostatecancer.health.blog/...
Hormonal therapies are one of the most important ways to manage PCa. prostatecancer.health.blog/...
kaptank in reply to
Great result. Long may it continue.
I notice you use dutasteride and finasteride concurrently with supra T. Being androgen blockers, do you think they interfere with the effects of the T? I found nothing about it in the literature but it just sort of makes sense to expel antiandrogens before injecting T. Just a guess on my part.
They (Avodart -- finasteride ) only lower DHT -- not testosterone -- and when taken w/o any ADT -- they actually raise testosterone ...
They are androgen blockers. Their effect on serum T is irrelevant because their main mode of action is to stop any T in the blood from reaching into the cancer cell. If you are doing BAT/supra T the aim is to expose the cell to large amounts of T. How can you do that if the cell is surrounded by a chemical ring of steel? Pour as much T in as you like, but it can't hit the target while androgen blockers are doing their work. At least that's the theory.
neither Avodart or finasteride are blocking the cells from getting testosterone -- nor are they blocking you from making testosterone -- they only keep you from converting testosterone to DHT. You make testosterone and all cells can and do use it. finasteride is propecia -- its is used for the treatment of male pattern hair loss. it doesn't stop you from making or using testosterone -- it doesn't even lower your testosterone....
Exactly. Dutasteride, finasteride, bicalutamide, enza and abi etc etc are all androgen BLOCKERS. They work in different ways, but all of them have a net effect of stopping androgens (incl DHT) entering the PCa cell, irrespective of the way the androgens might have been introduced into the body. By and large they have minimal effect on serum T. As opposed to ADT (lupron, zolodex etc) which stops the actual production of T in the body.
kaptank,
Avodart and finasteride are NOT testosterone blockers ---bicalutamide blocks testosterone from getting in cells -- lupron stops you from making testosterone -- but neither Avodart or finasteride keep you from making or using testosterone.
Exactly. Dutasteride and finasteride are in actual fact, classified as androgen blockers and always have been. They are less powerful than the 1st (eg bical) or 2nd generation of androgen blockers. One (of many) of the mechanisms by which they tend to work is to block, one way or another, androgen receptors on the PCa cell from engaging with androgens. They have no (or little) effect on the body's ability to make T. Unlike lupron and the other androgen DEPRIVATION agents. That is why, when ADT fails, we look at BLOCKADE agents to have in addition to simple ADT. Hence the term "triple blockade" for combinations of ADT and various blockers, like dut and fin and some of the other early zero generation ones (eg flutamide). Today, best SOC looks to use 2nd generation blockers (eg enza or abi) in conjuction with simple ADT.
Let's be clear about why I raised this. I don't know the answer and cannot find it in the literature. If you are trying to expose your cancer cells to levels of T that are toxic to it (and many mechanisms may be involved) then it seems you are just working against that aim by having androgen blockers running through you body whose main aim and purpose is to deny the cell access to any T that may be floating around. It is a point of importance to those who take dutasteride because it has a long half life and it takes 6 months to clear it from your system. That is why I don't take dut, I suspect (but do not KNOW) that it is incompatible with supra T type treatments because of it's long half life. I do take bical and stop it and wait a month before injecting T. It should have mostly washed through by then.
The lutamides are medically classified as androgen blockers.
As I said --- Avodart and finasteride are NOT testosterone blockers ---bicalutamide blocks testosterone from getting in cells -- lupron stops you from making testosterone --
but neither Avodart or finasteride keep you from making or using testosterone.
Neither one blocks androgen receptors on cancer cells or any other cell.
It simply lowers my DHT level to around 15 to 20 -- I still make DHT I still make testosterone and all the cells in my body get and use DTH and testosterone --- my testosterone level is 450 to 550 ... I have to stick with my doctors on this.
Depending on the amount of finasteride you take -- determines the level of DHT you make --- just like lowering cholesterol -- you don't stop making it and you don;t stop using it and no cells are blocked from getting cholesterol .
We are quibbling about terminology and angels on the heads of pins. 5ARIs are DHT inhibitors which makes them androgen blockers.
there is a significant difference between what I said and what you said -- but be that as it may ... no one would take finasteride simply to grow hair on their head as it is commonly prescribed -- if it cut off their testosterone or their bodies ability to use it or even lowered it--- thats for sure...
LOOK BOYS:
Some of you may qualify to go on intermittent HT, that is one goes on a three to up to six months combo, then stop all drugs, take your psa month and only go back on another round when your psa gets back up, again, best for starter guys with reoccurrence but works great for some guys.
ALSO, remember, with advanced prostate cancer, with NO known cure as of today, you are simply buying time on the planet. YOUR choice on how to spend your last days, but I strongly urge against stopping lupron-as much as too hate it, it has in part kept me alive for the past 20 years!!!!!
Also, at some point, lurpron stops working, and then the last stage starts with a finite end time.
You may have some reduced quality of life but you can still live a lot so do NOT stop taking meds. If you are lucky, you must just be still alive when they finally make apc a chronic disease, not the killer it is today.
LIVE LARGE, LIVE WELL, LIVE LONG-as long as you have quality of life.
I lost several pals who quit meds far too early and are now DEAD!!, -so I can still play with my grandson, ride my bike-not far now, still look at nice butts at the mall, enjoy ice cream, have a beer once in a while, so why would I give that up and die early, just because I cannot get it up -which with injections, pills etc. does still work sometimes,
More to life than a hard on boys, and lets face it, how good do we look, gee droopy old farts, if were lucky, so keep at it!!!!!
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