Not exactly a ringing endorsement for either if one is looking to Live Long and Prosper.
offering a better quality of life but not a cure
High T and BAT - Morgenthaler Harvard - Advanced Prostate...
High T and BAT - Morgenthaler Harvard
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Scout4answers
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Seems to work for some. Stage 4,G9/10, I think I will leave it alone. Life is Good , even with no T.
So does the study deal with the issue that high T and BAT seem to work very well for some people, and not at all for others?
When and if I come to this decision point, I think I will likely do an N=1 trial, and try 2 rounds of BAT.
Either it will work for me, or not.
If not I move on. If it does work I go for another few rounds, then try 3 months of straight high testosterone.
All the while getting weekly or biweekly PSA tests, and maybe a scan or two.
I just don't see a lot of risk with this approach. Either it will work, or if not I will catch it not working early and shut it down.
In the meantime it gives me some calendar time to run around and get lots of second opinions.
What do you think?
My only goal now is to avoid CRPC.
The results of Mergenthaler's most recent study are disappointing to me.
His focus on quality of life in his conclusion says it all. Not a potential cure for every one or he would be shouting it out loud.
What Patrick posted about is far more interesting to me at this point .
NF-κB Signaling Promotes Castration-Resistant Prostate Cancer Initiation and Progression
Quality of life has a nice sound to it
Scout4answers• in reply to
Maybe at 94, at 73 I want it all.
Not meant to offend but simply explain my thoughts of life/living/enjoying and screw the worrying
Anomalous wrote --- "Quality of life has a nice sound to it"
Scout4answers wrote --- "Maybe at 94, at 73 I want it all."
A possible reduced QUANTITY just to have GREAT QUALITY = my *no brainer choice*
I will be 71.5 years old in 5 days. This morning at 3:20AM I began a 28.82 mile bicycle ride. YESTERDAY at 3:56AM I began a 23.32 mile ride. My left shoulder is still recovering from a rotator cuff tear from a bicycle crash at mile 100 of 102 miles ridden on my JULY 4th SOLO ride last year. It's almost 7 years since diagnosed GL 10 at the time no extra, invasion or mets = lucky me.
I chose CASTRATION and not ADT
I chose cryoablation and not a SOC protocol
I chose a 3 drug non-FDA approved immuno injection as an experimental procedure
AND
I began bi-weekly Cypionate injections in JANUARY 2016 that results in 1,600ng/dL the day after injection and drops to 500/600 before the next injection then back to 1,600. I can VACATION for an extra 2 weeks resulting in 20/30ng/dL readings.
While others write about it -- I AM LIVING IT.
Pays your money and TAKES your chances since we all will die but I'm going out ON FIRE.
Way to go a2c!
You are living now while others accept a limited quality of life.
It is a choice we all have before us. It is what each of us is comfortable with accepting.
Currumpaw
Instructions to the Firing Squad? Remember members, the success to this procedure is to let go with your weapons on the words ON FIRE........... (Any left over cigarettes or butts are up for grabs)....
(Chonia Pola - JOHNS)...
Good Luck, Good Health and Good Humor.
j-o-h-n Friday 01/07/2022 5:15 PM EST - Greek Orthodox name day for JOHN.
your an inspiration a2c. Im presently on lupron and darolutamide along with 5mg of osterine and 5mg of caradarine and I feel fantastic especially when i hit the weights. It’s benn 3 months on this routine so far. I know daro and lupron will fail but hoping to block the other pathways to resistance just need to figure that out.
started 5 mg each RAD 140 and Cardarine 2 weeks ago and I can now lift same weight but 30 % more reps. This stuff makes a huge difference. I was struggling two weeks ago with each rep.
Only concern is my blood pressure has risen.
high blood pressure is not supposed to be a side effect only low HDL which cardarine should be taking care of.
Your heart is probably getting stronger also as it is a muscle.
Maybe you shouldn’t take your BP during workout lol.
Your
read somewhere that low HDL is a cause of high BP
we have to keep an eye on it. I think ADT is also a cause for poor heart health .
Why would you choose castration if testosterone may not , at least according to Morgenthaler be the problem….?……and now, even though you got castrated, go back on the very thing that castration destroys ? I’m cornfused here…..
*In 2015* SOC treatment via Urologist's instructions was to immediately start ADT Drugs but I requested the Orchiectomy. Chose Dr. Onik for treatment protocol and he said testosterone injections would begin following treatment.
Might be a type of holiday or vacation. With no downside to going back on ADT. My MO said the data shows intermittent ADT is a little less effective than continuous, but not all that much, so it seems to me holiday BAT might be a consideration. Then if PSA goes way up, just go back on Lupron. And maybe do it again sometime later
Scout4answers• in reply to
I agree, I was hoping that Sartor the Doc at Tulane was on to something when he therorized that one could keep this going indefinitely.while your quality of life is better you end up at the same place at about the same time …the dreaded CRPC.
Have not ruled it out, just disappointed in his results.
• in reply toScout4answers
Yeah I think its the kinda thing where you get so depressed and achy and brittle that you just say fugg it I want to feel a little better and i’m willing to knock a few months off the back end. Its an interesting video. Thanks for posting it.
I am encouraged - the risks of T have been overblown. Ordinary T therapy (T replacement) is probably not that useful to slow PCa (not fatal either) but supra T is another thing. There is a problem with his BAT methodology. He does couple of months of supra T (400mg every 2 weeks) followed by a couple of months of enza, then repeats. Problem is enza stops supra T from doing its work and stays in the system for a month or so. I think it would be more useful to just use ADT all the time to get to castrate levels. Then, after 6 months or so, do a period of enza (with ADT). All the evidence points to BAT potentiating enza after the BAT or reversing castrate resistance to enza. I don't see any point in doing BAT at the same time with enza - they work against each other.
But, more evidence that T is not fuel for PCa. We are still learning on this one. We don't yet know optimal periods and sequencing.
Sorry for ignorance, what is BAT? I’m new and wish that there was a list definitions for all the initials that are discussed.
There is. Try posts/pinned/ You will fund a post with a list of abrev. Welcome on board! It's all a part of the learning curve.
Scout,Much of what I had read points out to an extension of time for Castration Resistance from BAT. Morgantaler didnt discuss this. I think I first saw this video in mid-2020?Perhaps the evolution of thinking has changed?
Mike
Mike this was the most recent of his that I could find.
As I recall this talk was 3 mos ago. He has several on U-Tube
Right, it´s a disappointment. Other studies have shown better outcomes, with other patient sets. Being BRCA2+ which is supposed to predispose for better results on BAT, I am considering it. However, I have no evidence of disease now, with PSA undetectable, and all studies, even on the hormone-sensitive, have patients with PSA at the outset.
Full paper from last July:
liebertpub.com/doi/10.1089/... -Patrick
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Discussion
To the best of our knowledge this is the first reported clinical series in the PSA era of outcomes with TTh specifically in men with BCR or MET in a clinical setting, and not part of a formal trial. A total of 20 men with nonlocalized PCa and two receiving ADT deemed at high risk for metastases received TTh for up to 7 years with a median duration of >1 year, with considerable subjective improvement in quality of life, and without rapid progression, morbidity, or death. There was only one PCa-specific death during TTh, occurring 11 months after initiation of TTh in a 94-year-old man with diffuse metastases and initial PSA 546 ng/dL. Although this series of cases cannot establish safety of TTh in the setting of advanced PCa, these results do challenge the long-standing assumption that even transient exposure to increased serum T in a man with advanced PCa-with testosterone flare, for example, will rapidly precipitate morbidity or death.15
The original basis for the belief that TTh is dangerous for PCa arose from the work of Huggins and Hodges, who in 1941 concluded that “Testosterone injections cause activation of prostate cancer1” Contemporary review of their original data revealed it was based on erratic acid phosphatase data for only 14 days in a single hormonally intact individual.16 Fowler and Whitmore reported 45 of 52 men who received TTh demonstrated an undefined “unfavorable result” within 30 days; however, all but four of these men had already undergone castration or were on estrogen treatment to suppress serum T.2 Of these four men, three demonstrated no unfavorable results despite daily injections of T propionate for 51, 55, and 310 days. The appearance of poor outcomes for men on ADT but not for men who were hormonally intact inspired the development of the saturation model, which demonstrates a finite capacity of androgens to stimulate PCa growth, with exquisite sensitivity to changes in androgen concentrations at low values, and then insensitivity once the saturation point is reached,9 which appears to be ∼250 ng/dL in men.17,18 This study provides suggestive evidence for saturation in nonlocalized PCa, since men with BCR failed to demonstrate precipitous increases in PSA despite substantial periods of TTh.
There is scant literature regarding testosterone administration in men with advanced PCa in the PSA era. Leibowitz et al. reported results of a variety of strategies involving TTh in a mixed population of 96 men with PCa, of which it appears 31 likely had metastatic disease.19 Clinical trials of BAT in men with castrate-resistant prostate cancer reported a PSA decline in 7 of 14 men, and evaluable disease was reduced in 5 of 10 men.12 To optimize the duration of time on TTh, mBAT was developed13 and was used in seven men in the MET group in this study.
There are several notable observations from this clinical series. First, there exists a set of men for whom quality of life is more important than duration of life. Each patient understood that their choice of TTh could cause immediate or hastened disease progression, morbidity, and death. Second, these men only continued TTh because it provided them with symptomatic benefits to a degree that made it worthwhile, in their estimation, to risk their lives. This defies a frequently made assertion that TTh provides only minimal symptomatic benefits.20 Nearly all men experienced increased vigor. Sexual desire and ability were improved in many, and several were able to resume sexual activity after years without it, especially those on ADT. One man gained enough strength to give up the need for a walker. Several men and their partners noted a return of their “personality.” One regained fluency of speech and brain processing that had been severely compromised by ADT. Further research in this area would benefit from use of validated instruments to address subjective response to treatment.
Arguably the most important observation from this study is that TTh was not associated with rapid disease progression. Among men with BCR, with median duration of 33 months of TTh, only one progressed to metastatic disease >5 years after beginning TTh. This compares with 3 years estimates of metastatic disease in men with BCR after RP of 14% for Gleason score 5–7 and 37% for Gleason score 8–10.21 Hruby et al. reported that 70 of 538 men demonstrated biochemical failure after XRT for localized PCa with median follow-up of 50 months. Of these 70 men with biochemical failure, 13 had died and metastases were observed in 5 of the remaining 57 (8.8%).22 Only 30% of men with MET demonstrated progression on follow-up imaging studies by 3–12 months. The overall survival of 79.6% (mortality 21.4%) in the MET group compares with median survival of 47.2 months in the ADT alone arm of the CHAARTED Trial.23 The relevance of the short median PSA doubling times of 8.9 months in BCR and 4.4 months in MET is uncertain, as PSA doubling times are not usually determined in men receiving androgens, particularly since PSA expression is itself androgen-dependent.24
There are several important limitations to this study, including its retrospective nature, multiple forms of TTh treatment, and small sample size. In addition, PCa is a heterogenous disease, and this report includes those with Gleason scores ranging from 6 to 9, which may cloud interpretation of results. Nonetheless, these preliminary results indicate that TTh does not appear to cause precipitous PCa progression in men with BCR and MET. There may be a role for TTh in selected men with BCR, MET, or high-risk disease willing to accept the theoretical risk of hastened disease progression in return for enhanced quality of life.
Conclusion
TTh in men with BCR, MET, and high-risk PCa was associated with symptomatic benefits and low rates of complications, although interpretation of these results must be tempered by small sample size and a heterogeneous population. Well-designed prospective studies are needed to provide better evidence for the potential use of TTh in similarly affected individuals. In the meantime, these results may provide clinicians with a framework to counsel patients who prioritize quality of life over longevity.
Interesting post! I read a book by Dr John Lee in which he insists that the real culprit that is feeding PCa is E2, not T. ADT reduces T, but in reducing T it also reduces E2. Could it be possible that we should be concerned about managing E2 (Estradiol) instead of all this focus on T?
There are a number of conditions where the E2:T ratio has been singled out as being more significant than E2 & T separately. T begins to fall a little each year from our early 30's, which can ultimately lead to fat accumulation. Visceral fat secretes E2 and, at a certain point, the body lowers T to try to control E2 - & that worsens the situation.
Personally, I believe that doctors should try to reverse a poor E2:T ratio before chronic conditions, including PCa, emerge.
The focus on T is because castration is effective - for a while.
When Charles Huggins was making his name, male life expectancy was pretty bad in the U.S.. These days, a newborn male has an excellent chance of reaching age 65, and for those getting there without significant morbidity, another 20 years is not unreasonable. Castration is a two-year fix. Three years if you add Abi/Enza. Clearly inadequate in the modern era.
I have known a good number of men who have requested Arimidex, only to be told: "That's for women!" Denmeade, Morgentaler & even Dr. Myers seem unconcerned by E2.
-Patrick
I thought I read somewhere that Huggins found that high doses of T were just as effective as the lowering of T, in the suppression of PCa. Do you know if this is true or just our wishful thinking.
I seem to recall that he had some success with high-normal T after men became resistant to DES - i.e. CRPC.
Clearly we are in the infancy of BAT, and mBAT.WE NEED TO PAY ATTENTION to guys like A2C, and RSH1, Mateo Beach (Paul), and others. Nal talks about mixing it up, and keeping PCa in a state of confusion so it cannot figure an end run around. We are probably on to some form of progress. Still not curative, but progress.
A little of this, a little of that. Some combo may buy us a decade. Years, not months like so many of these crazy drug studies.
Mike
keeping PCa in a state of confusion so it cannot figure an end run around
That is what I am looking for, years not months.
From your profile - did you meet with him?
Can you pay for this out of pocket?
Dr Deagan McHugh, Oncologist + Dr Jonathon Coleman, Surgeon and first Clinical Trial (Phase 1) of NANO KNIFE (IRE- Irreversible Electrical Proation). Said No to Trial as Intermediate PCa only. I am Advanced PCa Stage 4. But…said he would agree to meet with me and see if there was something he could do.
9 mo ago I commented that I would leave this treatment alone... Now I am approaching my 3 mo. on it. Feel good, but PSA has been climbing so far... 3 mo, then scans was the plan... now scan lined up for the 2 mo. pt. PSMA scan to maybe get me on waiting list for Lu-177 in Seattle. We shall see. Third injection coming up a week after scan. Then time to review results and decide if going back on Enzo may be right. Don't know and never will know what decision was right. Feeling good now.
Will that be your first PSMA scan?
Its very sensitive. Got my first about a month ago and it looked like I never had any treatment these past 3 years. Very sensitive scan.
Yep,, first PSMA scan... normal bone and CT showed 4 new mets 3 months ago after 3 Ra-223 infusions... didn't do as well as hoped...
If approved I will be going into a trial with Docetaxel and the possibility of Ra-223 added (unblinded so I will know if I got the Ra-223 or not).
In any case hoping I get the radium and hopefully better results than you got.
For part of the trial pre-requirements I am getting a traditional bone scan and CT Wednesday. Will be interesting to compare to the PSMA a month ago which looked like my metastasis at the time of diagnosis of 1621 PSA and skull to shins bone mets. Looked like I never had the chemo and Zytiga these past 3 years. PSA now is probably 28 or so. Was 12 at time of PSMA scan.
We never know what decision is right without the benefit of hind sight.
As I remember some get a spike in PSA before it levels out.
Hoping for it to level out... then it would be continued....
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