"We have answered the questions and closed the book."
As reported in 2003, the risk for prostate cancer over the initial 7-year study period was 25% lower with finasteride than with placebo. That risk reduction now "goes out to 16 years, at least," (unlike ADT that quits working and causes mutations)
There is an "astonishing" level of interest in the prevention of prostate cancer, said Thompson. Clinicaltrials.gov has a long list of agents under investigation, such as metformin, statins, aspirin, and green tea.
But none of the studies, which are all relatively small, will ever be as authoritative as the PCPT. "You can prevent a quarter of all prostate cancers with finasteride," he pointed out.
"The chemopreventive agent, which is now generic, costs about $48 to $108 a month."
I would think all people doing BAT should take Avadart to block DHT from being produced..
(I’ve been taking T injections to get my T levels back up to high normal and occasionally SPT and taking Avadart for over 5 years... I have never taken any type of ADT since surgery over 6 years ago and my PSA runs between 1.7 and 2.4 (depending when I had the weekly injection and the day of the blood draw). My Post surgery PSA was 0.03 and went to 0.8 in 8 months then the doubling time slowed to over 20 months once I started taking one Avadart 3 times a week – (now taking one daily)
It is possible if not likely that the slow imbalance of low T and high DHT caused from aging is actually what leads to prostate cancer.
This would explain why the 25% lower incidence of prostate cancer by merely blocking DHT...
also notice – (a) no one became CRPC and (b) there were fewer PCa deaths in the finasteride group.
The median follow-up of trial participants was 18.4 years, and the cumulative follow-up was almost 300,000 years.
25% less prostate cancer in finasteride arm.
fewer prostate cancer deaths in the finasteride group than in the placebo group (42 vs 56).
RCT trial involved 18,000 + noncancer patients over 7 years with 18 year followup.
Can prostate cancer be prevented?
June 17, 2009/2011 Harvard Medical School
By merely taking Finasteride daily lowered the incidence of prostate cancer by over 25%
and extended the doubling time for those who had prostate cancer.
Nearly 19,000 men, ages 55 and older, enrolled in a seven-year landmark study, dubbed the Prostate Cancer Prevention Trial (PCPT), to determine whether the drug finasteride (Proscar) could prevent prostate cancer. The choice of finasteride, typically prescribed for the relief of urinary symptoms associated with an enlarged prostate, was based on two observations:
1. Male hormones, or androgens, drive the development of prostate cancer. Two common androgens are testosterone and the more powerful dihydrotestosterone (DHT).
2. Men deficient in an enzyme called 5-alpha-reductase type 2 don’t develop an enlarged prostate (also called benign prostatic hyperplasia, or BPH) or prostate cancer.
Fifteen months before the trial was scheduled to end, the independent Data and Safety Monitoring Committee, which tracks the health of participants, stopped the study because the evidence to that point was so striking: among those who took finasteride, the prevalence of prostate cancer was reduced by 24.8%. But the excitement was tempered by the fact that a higher percentage of men taking finasteride had aggressive tumors than men in the placebo group — 6.4% versus 5.1%. (See “Initial PCPT findings,” below.) Given the divergent findings, few doctors prescribed finasteride for prostate cancer prevention.
(even if initial findings stood – 1.3% vs. 24.8% less cancer overall – is not even a close call... 25% less cancer in the finasteride group held up over 16 years.
It would even be different if after 7 years t everyone in both groups got the same amount of PCa (ie, held it off for 7 years) – but that was not what happened – @ 16 years there was still 24.8% less in the finasteride side who never got PCa at all .
The common mistake I think everyone makes is to assume that ADT does the same thing.... but it does not.. ADT causes mutations and leads to CRPC over time. ADT blocks the ability to make T entirely and consequently use T entirely. So, yes, ADT stops DHT but stops everything else too – leading to many side effects heart / bone loss/ dementia etc. . Casodex blocks the cell receptors so they cannot get T entirely also. Avadart /finasteride only blocks the ability to convert T to DHT and allows the body to make and use T consequently no CRPC / bone loss/ heart / dementia etc.
M D Anderson admitted that ADT does not extend OS or cure PCa. But finasteride can actually prevent PCa and likely help in the treatment by slowing progression without causing CRPC.
If and when I progress to BAT – when I go on “vacation” I will still be taking Avadart to block the DHT.
I think the first phase BAT should be taking SPT for doublestrand breaks and then stopping T injections – the T will drop to zero in a month or so without taking any type of ADT – just like it does with estrogen patches in place of ADT– then start the T injections again in a couple of months... back and forth.
Finasteride costs $5 for 1 mg/day through goodrx.If you can afford 5 mg/day it is $6.
The government did a large study on Avodart (dutasteride). A somewhat more potent 5ARI. A month of 0.5 mg tabs is about $14 through goodrx.
1. ARTS - AVODART After Radical Therapy for Prostate Cancer Study - Study Results - ClinicalTrials.gov clinicaltrials.gov/ct2/show...
I think that with SPT or BAT we might not want to use 5ARIs during high T. I might use finasteride during the low T portion of BAT. Dutasteride has far too long of a half-life.
Background AVODART After Radical Therapy For Prostate Cancer Study (ARTS) reported dutasteride reduced PSA doubling (PSADT) at two years by 66% and disease progression by 59%. The durability of the cancer control is unknown.
Objective Explore the impact of dutasteride on PSADT and time to progression in men with PSA-only recurrent disease.
Design, Setting and Participants Retrospective examination of the impact of dutasteride on PSA kinetics and time to progression with PSA-only recurrent prostate cancer.
Intervention Dutasteride daily.
Outcome, Measurement and Statistical Analysis Change in PSA over time was determined by linear regression of natural log of PSA versus time. The slope of that curve was used as a measure of exponential PSA progression. Impact of dutasteride on slope was analyzed using Wilcoxon signed-rank two-sided test. Time to progression was analyzed using Kaplan-Meier, univariant and multivariant Cox regression.
Results and Limitation Compared to men with BPH, patients showed little change in PSA during the first 3 months. Thereafter, the PSA resumed an exponential increase. PSADT was 10.3 months pre dutasteride and 24.8 months post dutasteride. Multivariant analysis showed a strong correlation between post dutasteride PSA kinetics and time to progression, with close to 50% relapse free at 10 years. Post-dutasteride, patients with PSADT >9 months had significantly better survival.
Conclusions Dutasteride slows PSADT in PSA-only recurrent prostate cancer. This decline correlated with time to disease progression with close to 50% progression free at 10 years.
I still take dutasteride per Snuffy, it was part of his triple ADT approach - the multidimensional approach he called it. Shutting down numerous pathways and attacking it from different angles.
Lupron and Xtandi are the other two that make up triple ADT. I also still take Metformin and use estradiol patches per Snuffy. Estradiol is primarily for side effect of ADT, but it provides other benefits as well.
"Not on an iADT regimen. I am Active Surveillance directed by Dr. Myers. DHT went down from 105 to 4. PSA from 8 to 2.5. This included Metformin, several supplements, Med diet and exercise."
I like it.... you are more proof that Avadart works !
I might or might or might not be "proof." Everyone is different and he treated everyone in a custom fashion. I speak only about the impact me. I am sorry he is no longer practicing.
Using finasteride instead of dutasteride to avoid the problem of clearing dutasteride during BAT is so obvious I never would have thought of it. Many thanks.
But why? you are trying to eliminate DHT always and entirely -- it is the engine to PCa and PCa progression.... Avadart cuts off both avenues to converting T to DHT.
He already has PCa so he might decide that he wants DHT to be high during the high T phase and all androgens low during the ADT phase. If so, finasteride is the way to go. If you want to block DHT all the time, then dutasteride is the way to go (or both).
IMHO you should not want DHT ever... as the trial proved... with 18,000 men without PCa at the start -- resulted in 25%less cancer and it holds up @ 18 years and counting – and with no CRPC>
As for those who have cancer -- BCR after surgery or radiation – Avadart (blocks both pathways for DHT but leaves the testosterone for the body to freely use) caused 18% of their cases to disappear... and extended doubling time to over 2 years and no one gets CRPC -- See Snuffy Myer's study and his video posted on this thread..
Also see my reply to maley2711:
"Your past postings regarding whether to take ADT for BCR illustrate the same problem---and make / prove the same point.
from your previous post: "Timing of Androgen Deprivation Treatment for Men with Biochemical Recurrent Prostate Cancer in the Context of Novel Therapies"
"These data provide context for patients with BCR and providers on whether to undergo ADT for years despite unproven benefit and quality of life impact. New imaging may help or further add to the controversy, since BCR patients may have metastases on newer imaging. Until definitive data are available, men with BCR should be counselled regarding the lack of data to support ADT benefit in nonmetastatic BCR."
Clearly ADT is often not helpful.... and in many cases brings on CRPC years earlier --- whereas blocking ONLY DHT with Avadart -- and not blocking testosterone has proven long term benefits --- lower PSA doubling time to over 2 years and no CRPC developing even after 18 + years of follow up... And,of those who started Avadart when BCR post surgery /radiation -- 18% had their cancer disappear.
Clearly the science is that DHT is the problem-- not Testosterone. More importantly taking away both DHT and T have adverse effects -- proven by over 70 years of little actual benefit when all is said and done."
When I did straight ADT I used dutasteride and finasteride. As you point out for ADT or even physiological testosterone it seems like they might be beneficial.
But I'm doing BAT now so a completely different ball game. BAT is cycling SPT and ADT (high periods of androgen with low periods of androgens). DHT is an androgen and is 5 times as powerful as testosterone. During high testosterone, DHT studies show that it works better than straight testosterone. But ONLY for times where you are trying to take your androgens high - probably to introduce DNA double-strand breaks.
Unfortunately, there is no slam dunk RCT for BAT with 5ARIs that we can point to.
Personally, I don't think it would destroy BAT if you used a 5ARI as long as your free testosterone (or bioavailable?) is high. As Patrick said, "DHT is your friend until it no longer is". I don't think that I'm at the "no longer is" point (since my PSA on low cycles goes to zero). I don't know how to determine that point other than to try introducing a 5ARI when BAT starts to fail. Monitor what happens.
RSH1 has answered better than I could. I would only add that there is at least one mouse study supporting the avoidance of avodart during the high T phase of BAT. Sorry, I do not have a link at hand.
Working on the theory of using super levels of testosterone to shock PCa cells back to T sensitivity from mCRPC or nonmCRPC and continuing to cycle back and forth (BAT).... or BAT to cause non metastatic CRPC to have double strand breaks to kill a few PCa cells. Or BAT for HSPC as RSH1 is experimenting with... their body cannot convert the T to DHT during the on SPT cycle due to the ADT they are taking simultaneously.
Even if they were to stop the ADT when they take the SPT – the lingering effects of ADT blocks the ability to convert T to DHT for weeks.
As for RSH1’s trial cohart of 1, there is no MD support for that or his other “trials”. It is likely that the best approach he could have taken for BCR would have been Avadart and nothing else – It would be the least damaging and likely worked for many years while waiting for advances in science to a better treatment than ADT which will/has started the all too early treck toward CRPC.
The following article was posted by maley2711 2 months ago
"Timing of Androgen Deprivation Treatment for Men with Biochemical Recurrent Prostate Cancer in the Context of Novel Therapies"
"These data provide context for patients with BCR and providers on whether to undergo ADT for years despite unproven benefit and quality of life impact. New imaging may help or further add to the controversy, since BCR patients may have metastases on newer imaging. Until definitive data are available, men with BCR should be counselled regarding the lack of data to support ADT benefit in nonmetastatic BCR."
Published September, 2021
Conclusions
"Men with biochemically recurrent prostate cancer, who defer hormone therapy until metastasis have overall survival that is quite long and the early initiation of continuous androgen deprivation therapy for biochemical relapse, may not meaningfully improve overall survival. "
It is likely that anyone who is post surgery/radiation BCR and nonmetastic is better off on Avadart till mets appear.
Dr. Snuffy Myers recommends Avadart for BCR til mets show.-- he said it not only slowed progression -- in some 18% of cases of active surveillance -- the cancer disappeared.
One other thing that I found astounding in the articles listed (and probably missed by many) is one of the facts cited by the New England Journal of Medicine and the Harvard School of Medicine...for why they thought eliminating DHT ONLY was the answer.
Men deficient in an enzyme called 5-alpha-reductase type 2 do not develope BPH OR PROSTATE CANCER !
"Men deficient in an enzyme called 5-alpha-reductase type 2 DONOT develop an enlarged prostate (also called benign prostatic hyperplasia, or BPH) OR PROSTATE CANCER. Without 5-alpha-reductase type 2, testosterone can’t be converted into DHT, which promotes prostate growth. (See “Two enzyme types,” below.) "
"Because finasteride tamps down 5-alpha-reductase type 2, researchers hypothesized that it would lower DHT levels and help prevent prostate cancer."
and:
Two enzyme types
The enzyme 5-alpha-reductase comes in two forms: type 1 and type 2. Prostate growth requires both forms. Blocking the enzyme can help shrink the prostate gland and relieve the urinary symptoms associated with BPH.
Finasteride blocks type 2. Another drug, dutasteride (Avodart), blocks both types of 5-alpha-reductase. Blocking both types might seem like the most effective treatment strategy for BPH, and findings from recent studies comparing the drugs support this theory.
Hi George71;You write "It is likely that anyone who is post surgery/radiation BCR and nonmetastic is better off on Avadart till mets appear." For my n=1, both post-surgery and post salvage radiation and post radiation to common iliac and para-aorta I was taking dutasteride and my PSA was steadily climbing. So no way was I not going to do something. After the last radiation I had almost a year of climbing PSA while waiting for a clinical trial that kept getting postponed and finally abandoned. I already had tiny (a few millimeters) mets (hence the second radiation), but then, with even better scans, I would guess that almost anyone with a rising PSA (not due to BPH) has mets of some size. So the idea of only avodart until there are mets seems to me undesirable because, with a rising PSA, whether mets are present or not usually depends on whether our current scan technology is sufficient.
Don't start ADT till mets appear in regular imaging "irrespective of NARTD used in nmCRPC":
That is what the science says:
Retrospective review of men who underwent RP from1983 - 2014 within Johns Hopkins and the Center for Prostate Disease Research Multi-Center National Database, developed BCR and did not receive ADT until metastasis.
"ADT prior to mets may not improve QoL or OS in BCR prostate cancer and may result in irreversible adverse events at high costs. Early use of novel androgen receptor targeting drugs (NARTD) prolonged MFS in nonmetastatic-castration resistant prostate cancer (nmCRPC). However, clinical details prior to castration resistance and explicit criteria for starting ADT were not given. We hypothesize that deferring ADT until mets results in outcomes comparable to those reported with early ADT,."
"their body cannot convert the T to DHT during the on SPT cycle due to the ADT they are taking simultaneously."I did not know this. Why doesn't the 5AR enzyme work for exogenous bioidentical T?
Many doctors use Avodart with ADT (sometimes they do this as part of the so-called triple androgen blockage). Do you think that they do this to counter the DHT conversion during the T flare or before endogenous T goes low? It is important to note that T does not go to absolute zero - it can go to undetectable levels on our present tests and for many men, it is over 10 ng/dl. But then, why do they do it continuously? Is it for the men who still exhibit some endogenous T (100% of them are above absolute zero)? And another wrinkle is that your cancer cells are also busy producing T.
My MO supports my BAT trial and BAT has perhaps a half dozen or so RCTs supporting its use. There are a few in these links:
1. Bipolar androgen therapy (BAT): A patient's guide - Denmeade - - The Prostate - Wiley Online Library onlinelibrary.wiley.com/doi...
2. How BAT Works and possible BAT/Xtandi repeats
3. Bipolar Androgen Therapy for Men with Androgen Ablation Naïve Prostate Cancer: Results From the Phase II BATMAN Study – PubMed pubmed.ncbi.nlm.nih.gov/273...
4. Serial bipolar androgen therapy (sBAT) using cyclic supraphysiologic testosterone (STP) to treat metastatic castration-resistant prostate cancer (mCRPC) - Isaacs - Annals of Translational Medicine atm.amegroups.com/article/v...
9. Rapid Androgen Cycling as Treatment for Patients with Prostate Cancer | Clinical Cancer Research clincancerres.aacrjournals....
10. References in High-Dose Testosterone and Radium-223 Response in Metastatic Castration-Resistant Prostate Cancer - Clinical Genitourinary Cancer clinical-genitourinary-canc...
11. Breaking androgen receptor addiction of prostate cancer by targeting different functional domains in the treatment of advanced disease – ScienceDirect sciencedirect.com/science/a...
12. Rapid Hormonal Cycling as Treatment for Patients with Prostate Cancer: The Men’s Cycle - Study Results - ClinicalTrials.gov clinicaltrials.gov/ct2/show...
13. Rapid Androgen Cycling as Treatment for Patients with Prostate Cancer | Clinical Cancer Research clincancerres.aacrjournals....
14. Sci-Hub | Bipolar androgen therapy in men with metastatic castration-resistant prostate cancer after progression on enzalutamide: an open-label, phase 2, multicohort study. The Lancet Oncology, 19(1), 76–86 | 10.1016/S1470-2045(17)30906-3 sci-hub.se/10.1016/S1470-20...
15. Mathematical modeling of prostate cancer progression in response to androgen ablation therapy | PNAS pnas.org/content/108/49/19701
16. Sci-Hub | Strategies for Testosterone Therapy in Men with Metastatic Prostate Cancer in Clinical Practice: Introducing Modified Bipolar Androgen Therapy. Androgens: Clinical Research and Therapeutics, 1(1), 76–84 | 10.1089/andro.2020.0009 sci-hub.se/10.1089/andro.20...
19. Bipolar Androgen Therapy and the Immune System |
20. STEP-UP RCT. BAT, Enzalutamide, BAT, Enzalutamide, repeat.. Sequential Testosterone and Enzalutamide Prevents Unfavorable Progression - Full Text View - ClinicalTrials.gov clinicaltrials.gov/ct2/show...
21. RE-sensitizing With Supraphysiologic Testosterone to Overcome REsistance (The RESTORE Study) - Full Text View - ClinicalTrials.gov clinicaltrials.gov/ct2/show...
22. High testosterone gives rise to high DHT (approximately 10% of testosterone is converted to DHT through 5 alpha reductase enzyme (5AR)): High-dose-androgen-induced autophagic cell death to suppress the Enzalutamide-resistant prostate cancer growth via altering the circRNA-BCL2/miRNA-198/AMBRA1 signaling | Cell Death Discovery nature.com/articles/s41420-...
23. Sci-Hub | Effect of bipolar androgen therapy for asymptomatic men with castration-resistant prostate cancer: Results from a pilot clinical study | 10.1126/scitranslmed.3010563 sci-hubtw.hkvisa.net/10.112...
24. Home | Medical society dedicated to testosterone deficiency (hypogonadism) and its treatment androgensociety.org/
27. 5ARIs perhaps not beneficial: High-dose-androgen-induced autophagic cell death to suppress the Enzalutamide-resistant prostate cancer growth via altering the circRNA-BCL2/miRNA-198/AMBRA1 signaling – PubMed pubmed.ncbi.nlm.nih.gov/353...
28. 5ARIs perhaps not beneficial: Association between dihydrotestosterone and long-term risk for prostate cancer mortality: A prospective cohort study – PubMed pubmed.ncbi.nlm.nih.gov/323...
36. Mathematical modeling of prostate cancer progression in response to androgen ablation therapy | PNAS pnas.org/content/108/49/19701
37. Sci-Hub | Strategies for Testosterone Therapy in Men with Metastatic Prostate Cancer in Clinical Practice: Introducing Modified Bipolar Androgen Therapy. Androgens: Clinical Research and Therapeutics, 1(1), 76–84 | 10.1089/andro.2020.0009 sci-hub.se/10.1089/andro.20...
39. Finasteride upregulates expression of androgen receptor in hyperplastic prostate and LNCaP cells: Implications for chemoprevention of prostate cancer - Hsieh - 2011 - The Prostate - Wiley Online Library onlinelibrary.wiley.com/doi...
40. Sci-Hub | Aromatase activity in the breast and other peripheral tissues and its therapeutic regulation | 10.1016/0039-128x(87)90036-5 sci-hubtw.hkvisa.net/10.101...
41. Sequential High Dose Testosterone and Enzalutamide Compared with Enzalutamide Alone for the Treatment of Asymptomatic Metastatic Castration Resistant Prostate Cancer, STEP-UP Study cancer.gov/about-cancer/tre...
42. Strategies for Testosterone Therapy in Men with Metastatic Prostate Cancer in Clinical Practice: Introducing Modified Bipolar Androgen Therapy | Androgens: Clinical Research and Therapeutics liebertpub.com/doi/10.1089/...
My estrogen ADT was a trial but since that time the UK has done a very large RCT showing its efficacy (PATCH trial). Estrogen was the main SOC choice for 4 decades, so my trial was more of a historical rehash rather than a trial :). Interesting because some doctors that I talked to did not appear to be aware of that fact (or they feigned ignorance to push Lupron). If it wasn't for the fact that I don't think E should be high while T is high, I would do high E for my underlying BAT ADT. My T was undetectable 100% of the time when I used 0.3-0.4 mg/day of estrogen. This was one of the few times that my MO wasn't spot on. She didn't think my T would go to undetectable levels. To be fair, 3 other MOs I spoke with thought it just wouldn't do much of anything at all! I'm not sure if they really believed that or if they wanted me to follow today's U.S. SOC.
There is a lot of evidence in support of BAT. There is also evidence to support 5ARIs with ADT or normal levels of T.
I'm thinking that Patrick's quote is applicable as pertaining to our BAT discussions "DHT is your friend until it no longer is". So, no 5ARI until you need a 5ARI.
There are many opinions one way or the other but I choose to monitor my own progress. Then modify variables as needed to adjust my course. Seems the sane route to me since we are dealing with millions of variables and a heterogenous cancer that mutates on a regular basis.
One thing I notice is that much of what I read on this forum concerns BPH or the prevention of PCa. I already have PCa and it is advanced.
You asked: "Why doesn't the 5AR enzyme work for exogenous bioidentical T?"
June 17, 2009/2011 Harvard Medical School:
"2. Men deficient in an enzyme called 5-alpha-reductase type 2 don’t develop an enlarged prostate (also called benign prostatic hyperplasia, or BPH) or prostate cancer."
And don't become CRPC even after 18 + year follow up because their bodies keep making and using testosterone. Avadart only blocks the bodies ability to convert T to DHT... DHT is the driver of PCa not T. ADT cuts off both T and consequently DHT .. thus the short lived"apparent" benefit of ADT.... compared to Avadarts 18 + year proven benefit to lower cases of PCa by 25% and dramatically slow growth if you already have BCR PCa.
Avadart does work with exogenous bioidentical T (ie blocks the ability of the body to convert T to DHT) .. that is what they are saying in the articles --- ie. with nothing but Avadart PSA doubling time is extended 66% (from 10 months to 23 months for BCR after surgery and or radiation)
According to Johns Hopkins and and the Center for Prostate Disease Research Multi-Center National Database -- concluded that:
"ADT prior to mets may not improve QoL or OS in BCR prostate cancer and may result in irreversible adverse events at high costs."
And:
"Deferred ADT until time of metastases results in long MFS and OS even with short PSADT suggesting that it remains possible that prolongation of MFS in nmCRPC may not reflect true overall net therapeutic benefits which requires prospective study to define specific patient selection and criteria for initial ADT implementation, control of post progression management and QoL/OS information."
PSADT - < =6 months < =10 months
Median MFS (all) not reached 12 (8-16) years and 16 (15-21) years
Median OS 21 (20-22) years 14 (12-17) years and 17 (15-18) years
Avadart is what Snuffy perscribes for BCR after surgery/ radiation or chemo treatment ----- He prescribes Avadart during iADT for BCR ...(to stop any residual T from being converted to DHT) then when off iADT he continues Avadart daily to stop the body from converting T to DHT when their natural T returns.... ... In some cases he adds back T along with Avadart even in BCR active PCa... (as cited in his videos see below)
As you know: finasteride prevents prostate cancer by 25% -- and all it does is stops the body from converting T into DHT. and allows your body to make and use T (and extended the doubling time for those who had prostate cancer as shown in the ARTS trial. .
"Can prostate cancer be prevented?"
June 17, 2009/2011 Harvard Medical School:
RCT trial involved 18,000 + noncancer patients over 7 years with 18 year followup.
Nearly 19,000 men, ages 55 and older, enrolled in a seven-year landmark study, dubbed the Prostate Cancer Prevention Trial (PCPT), to determine whether the drug finasteride (Proscar) could prevent prostate cancer. The choice of finasteride, typically prescribed for the relief of urinary symptoms associated with an enlarged prostate, was based on two observations:
1. Male hormones, or androgens, drive the development of prostate cancer. Two common androgens are testosterone and the more powerful dihydrotestosterone (DHT).
2. Men deficient in an enzyme called 5-alpha-reductase type 2 don’t develop an enlarged prostate (also called benign prostatic hyperplasia, or BPH) or prostate cancer.
My thoughts are -- avoid ADT until necessary as per the science above: There is a time for BAT for HSPC but not until way down the road IMHO ... til then -- as shown above -- Avadart til mets show which is likely 12 years or more even in people with <6months doubling time -- then iADT for short 1 or 2 months then Avadart diet exercise supplements til PSA reaches 5 or so and go back on iADT for 1 or 2 months and off again to ensure no CRPC> it could be 4 or 5 years between iADT cycles -- see Snuffy's video.
As you noted every one of us is different.... In the recently posted article by Patrick – Denmeade said CRPC from continuous ADT occurs on average in 1 to 2 years ... that seems a little faster than what I have read,,, (2 to 3 years) but some men have been on continuous ADT for over 10 years !
But, once CRPC occurs the newer drugs when added fail pretty soon thereafter also.
Thus the BAT for CRPC to try and reactivate the drugs effectiveness.
I know they have shown some slowing benefit to BAT in HSPC – but my thinking is why go there till necessary --- avoid CRPC at all cost – (ie. take Avadart and nothing else -- til rising PSA to 5 - 10 range as long as no mets appear with regular imaging).
That will take likely more then 10 years – No mutating to CRPC years early... – no dementia / bone loss / heart problems from years of ADT... plus all the benefits of T.
We are trying to buy time – as you know, nothing currently can cure us except surgery or radiation of every last speck.... and there is no way to ever know if that occurs.... many cancers are indolent and go on for decades doing little to nothing meaningful with no treatment –
By the way .. I went back to M D Anderson (I had not been back there since 2019) for a consult about scheduling a PSMA scan since they are one of only a few in my area that currently does them -- they were all good with Avadart and supplements and offered no adjustment until PSA reaches 5 to 10 "whatever my comfort zone is" unless rapid doubling time and mets occur... He said they are rethinking the early ADT approach and think that positive PSMA scans may not trigger ADT use because many times people have a few small mets that they would not have even seen for 3 or 4 more years with conventional pet scans -- and they aren't sure just what to do ... "maybe zap them with radiation when they pop up if they are in a place where that is an option -- then stay on Avadart only and wait and see what happens" They told me to call when I was ready to schedule a PSMA scan and they would do it. I think it is about the doubling time (growth rate) if we can slow it to 2 + years and not do anything that mutates it into CRPC we can likely out live it -- Having a temporary zero PSA for a time on ADT may be detrimental to that goal since ADT can't cure you and causes many bad issues in other ways.
My thought is that by alternating high and low periods of androgens I might not ever go CRPC. If I do, I hope that Xtandi or a yet-to-be-discovered therapy works for me. As you said, BAT resensitizes most men to Xtandi. And a trial is underway to see if it can be repeated more than once. Danmeade thinks that it might be possible to continue indefinitely.
My cancer is rather advanced and aggressive. Mayo docs predicted 3 months max before I was in the hospital for chemo or radiation. That was in 2018. I view this as 3+ bonus years. Avodart works on guys with less advanced cancer. Unfortunately I am beyond that option.
I hear you about the constant ADT. I don't view that as a viable option. Unless I am in the endgame and ADT buys me the last year or so.
I misread your comment "their body cannot convert the T to DHT during the on SPT cycle due to the ADT they are taking simultaneously." and I thought you were saying that ADT somehow changed exogenous T and prevented the 5AR enzyme from converting T to DHT.
And when on ADT if your T is not absolute zero and/or your cancer cells are producing T then a 5ARI still works to block residual DHT. Is it needed is more the question. Some say yes, some say no. Patrick says no until it becomes a yes (I assume for SPT as well as ADT). He has been doing this successfully for many years and has biology to back him, so I will defer to him. I am only on month 8.
The title of this lengthy post says, “Finasteride Safely Prevents Prostate Cancer”. Does the data show it benefits th oh se of us who already have APC? If so could you provide the link to that data?
Dr. Snuffy Myers recommends Avadart for BCR til mets show.-- he said it not only slowed progression -- in some 18% of cases of active surveillance -- the cancer disappeared.
Dutasteride is similar. RCTs show possible benefit in some subsets of guys with PCa. I haven't run across an RCT for high-risk APC.
So much is in context. Perhaps there is a benefit if you are doing ADT or have normal or low testosterone.
1. ARTS - AVODART After Radical Therapy for Prostate Cancer Study - Study Results - ClinicalTrials.gov clinicaltrials.gov/ct2/show...
2. Feasibility of Hormones and Radiation for Intermediate or High-Risk Prostate Cancer - Study Results - ClinicalTrials.gov clinicaltrials.gov/ct2/show...
3. Prostate Cancer Study in Men Who Have Failed First-Line Androgen Deprivation Therapy - Study Results - ClinicalTrials.gov clinicaltrials.gov/ct2/show...
4. Assessment Of Dutasteride (AVODART) In Extending the Time to Progression of Low-Risk, Localized Prostate Cancer In Men - Study Results - ClinicalTrials.gov
It's likely why you were able to hold it off until you were 80 ! -- that's really good. you are likely to top 100 -- they will have better treatment soon.
Thanks. Sometimes I think the stars are misaligned. I was ignorant of what PSA indicated vs. BPH. Nearly 2 years before dx, I had lab work saying my PSA was 8.8. The PA didn't say anything about it. I thought my problems were because of BPH. Finally a new Dr. got me to a urologist and here I am. Statute of Limitations kept me from suing the PA. I try to tell as many folks as I can about PCa. In a RV Co-op, so a target rich environment.
Mine was 5.4 then went to 7.9 but no DRE to check the prostate then 2 years later bang went the symptoms and 116.9 PSA. What really did me in with the oncologist that it was in my chart I refused treatment which was untrue, could sue but what is the use now.
Sucks but the bright side is that you might help save some people. That's one of the ways I look at it. I coulda, woulda, shoulda caught it earlier. But catching it later means that I can spread whatever info I gather and maybe help someone else.
The dark side of the story above is that the FDA has also warned about the 0.5 to 0.7 percent risk of a high-grade prostate cancer diagnosis (G8-10) while using the drugs.
While that seems like a low number, that's on the order of one in every 200, and I believe that I am one of them. My [former] urologist convinced me to use dutasteride despite the warning and didn't do a biopsy as my PSA rose until I had a Stage 4 problem on my hands.
The study above is about its use in preventing cancer. It may well have a role once you are on ADT but I think the jury is still out on that.
You must not have seen the articles that addressed both of your concerns: (a) increased risk of high-grade prostate cancer and (b) used for treatment of prostate cancer after relapse from surgery or radiation.
concern (a) From the New England Journal of Medicine --- "The early concerns regarding an association between finasteride and an increased risk of high-grade prostate cancer have not been borne out." And: " Finasteride is a generic agent that is used to treat lower urinary tract symptoms, prevents complications from these symptoms, and PREVENTS prostate cancer.
This after: "296,842 person-years of follow-up and a median follow-up of 18.4 years, of over 18,000 men.
And concern (b) treatment of prostate cancer after relapse from surgery or radiation :
impact of Dutasteride on PSA Kinetics and Time to Progression in Men with PSA-only Recurrent Prostate Cancer:
Charles E Myers, Michelle S McCarthy
doi: doi.org/10.1101/2021.05.03....
Abstract
Background AVODART After Radical Therapy For Prostate Cancer Study (ARTS) reported dutasteride reduced PSA doubling (PSADT) at two years by 66% and disease progression by 59%. The durability of the cancer control is unknown.
Objective Explore the impact of dutasteride on PSADT and time to progression in men with PSA-only recurrent disease.
Design, Setting and Participants Retrospective examination of the impact of dutasteride on PSA kinetics and time to progression with PSA-only recurrent prostate cancer.
Intervention Dutasteride daily.
Outcome, Measurement and Statistical Analysis Change in PSA over time was determined by linear regression of natural log of PSA versus time. The slope of that curve was used as a measure of exponential PSA progression. Impact of dutasteride on slope was analyzed using Wilcoxon signed-rank two-sided test. Time to progression was analyzed using Kaplan-Meier, univariant and multivariant Cox regression.
Results and Limitation Compared to men with BPH, patients showed little change in PSA during the first 3 months. Thereafter, the PSA resumed an exponential increase. PSADT was 10.3 months pre dutasteride and 24.8 months post dutasteride. Multivariant analysis showed a strong correlation between post dutasteride PSA kinetics and time to progression, with close to 50% relapse free at 10 years. Post-dutasteride, patients with PSADT >9 months had significantly better survival.
Conclusions Dutasteride slows PSADT in PSA-only recurrent prostate cancer. This decline correlated with time to disease progression with close to 50% progression free at 10 years.
ALSO see the video link below:
18% of men treated with Avadart -- after PSA relapse post surgery / radiation -- had their cancer disappear.
I used it and wound up with Gleason 9. I'm not sure the Avodart was causative. The worst thing about Avodart is that it masks the true PSA. I went to my GP and he did routine PSA tests that were in the high normal range. Then I felt like something was wrong and I went to him and he said "it wasn't time for my yearly PSA test" but I insisted. The PSA came back at around 8.0 and I was immediately sent to a urologist who told me about the Avodart effect. He did a biopsy and here I am--a member of a club that no one wants to belong to.
it was at the suggestion of my GP. I was on Flomax and Avodart. I was ignorant obviously and had no thoughts of Pca even though my grandfather died from it. I received annual tests plus the digital exam. I knew nothing about BRCA2 or anything really.
It is likely (given the 18 year trial results cited here that includes 18,000 + men and 300,000 man years) that Avadart helped slow the progress of your cancer. It extended the doubling time nearly 2 years .
Without the Avadart your cancer would have likely progressed much faster and you would have reached the G9 several years sooner. Avadart lowered my PSA number by about 25% -- the PSA number is just relative to its doubling time.... many men have PSA of 30 and don't have PCa. If it takes 20 years for my PSA to go from lets say 5 to 30 --- I will never know I had PCa.
On the other hand -- ADT lowers PSA from 200 to zero ... making one think the cancer is doing nothing -- but in the case of ADT (because it knocks out all your testosterone along with DHT) the cancer is mutating toward CRPC>.... at least that didn't happen while on Avadart.
There is a paper by David Crawford that I can't seem to find in which he discusses the use of dutasteride to prevent prostate cancer, and the two takeaways that I have in my head are: 1. if your PSA doesn't drop by at least 50% when you start taking it, suspect PCa, and 2. if your PSA rises at all while on it, you should do a biopsy.
Great news ! --- It's been working for me too. All evidence points to DHT being the problem -- not T.
I think the evidence shows that cutting off T causes CRPC.
I think the evidence shows that simply low T (along with rising DHT) which is what happens gradually over years in all old guys is likely what brings on PCa in the first place.
Young guys almost never get PCa and they have high T and low DHT ratio, Old guys gradually have lowering T and rising DHT year over year till PCa sets in.
Nal, why are you taking both drugs when they seem to have very similar mechanisms of action? If you were to take one only, which would you choose? Thanks
If I had to attribute my stalled PCa progression to any thing it is Avadart... It is the only thing I've done other than supplements and minor diet changes -- no eggs (choline) eat more fish / boron / melatonin
I started injections -- about 2 years ago (prior to that I was just allowing my T to be in natural range (around 450 to 650 -- naturally.... and only taking Avadart to stop DHT.... along with the other supplements we all take D3 / 10,000 daily K / curcumin /grape seed extract/ Quercetin / etc etc)
As you know I had PCa in 4 of 10 lymph nodes post surgery and 0.03 PSA in April 2016
Gleason 4+4=8 or 4+5=9 depending on whose opinion to believe -- I followed Snuffy's advise -- all others wanted to put me on ADT immediately and do radiation in the blind.
Until 2 years ago Avadart alone had kept my PSA almost static at 0.8 to 1.1 for around 4 years. (PSA doubling time over 20 months) Actually It never doubled once in the 4 years..
I am including the following details which likely account for some of the changes in PSA etc.
Just prior to the Covid19 outbreak I signed up for a immuno threapy trial @ NIH -- it was canceled before I could even begin -- but --- I had to get off of the Avadart for a 6 month lead in.... during which time my PSA went up from 0.9 to 1.47.... Had it not gone up I could not have qualified for the trial - it had to be increasing at a doubling time of between 9 to 15 months.
If I haden't tried to get on the trial I think my PSA would likely still be around 1.2 or so with nothing but Avadart... it is currently between 1.7 and 2.4
After the trial was cancelled, I decided to try CONSTANT Super T (not BAT) to see if I could get double strand breaks as per Denmeade / Dr. Bob / Dr. Kahara etc. and just keep the cancer plugged up and unable to replicate -- on the premise that PCa cells have to expel the T from the nucleus in order to complete the cycle and divide.
I started taking 1 cc T cyp per week --- it initially jumped my T up from around 500 to over 3500 and PSA went immediately to 2.2 from 1.47 (Sept 2019) -- then three months later PSA went down to 1.2 -- (I was still on constant super T -- taking one cc injection weekly -- it kept me over 3500 T). Then after about 8 months -- I concluded that maintaining constant super T wasn't doing much if anything, other than keeping PSA constant @ around 1.7 to 2.4 -- so I concluded that constant super T wasn't helpful and reduced T to weekly 1/3 cc. injections about 4 months ago. (to try and get back to normal range) --- 1/3 cc gets my T to a high of about 800 (right after the shot) and a low of about 350 to 400 just prior to my next (weekly) injection of 1/3 cc.
I would like to stop the injections and go back to natural T levels as before -- but stopping the injections will result in an unknown period of super low T until my body realizes there is no T and begins to start making it again naturally. When I laid off the T injections for one month -- to get my T levels back near normal -- my T went from 3500 + to 146 and my PSA dropped to 1.05 from 2.4 ...
After about 8 months of constant super T and constant T levels of over 3500 -- I began to have high hematocrit 49.3 . The Dr. said there was no problem unless it got to around 60 -- but to relieve my concern -- he sent me to give a pint of blood which dropped it back to 46 three months later.
It seems to me that (unless someone has unusually low T levels) they should not take T --- just take Avadart ..... unless PCa progresses to the point that they need to do BAT... then they should probably start with 1 cc T cyp weekly for 2 months to cause the double strand break then stop the T entirely and their PSA will drop like a rock without the need for ADT -- just like the estrogen patches do -- without ADT. The estrogen patches make the T go to nothing and the PSA goes to nothing also -- all without the negative effects of ADT. The PSA will drop to nothing and the T will drop to nothing by simply stopping the T injections.
My experiment with constant super T proved to not help me much, if at all .....
On the other hand I think I would try BAT with DAILY AVADART (for life) and alternating 2 months of super T (1cc weekly) followed by two months of no T and then take 1/3 cc weekly and daily Avadart until PSA went back up to where it was at the start of the BAT cycle -- which could be months or years.... and repeat.... It would likely take a decade or more OR NEVER become CRPC . I think many try to get to a PSA of zero and in doing so stress the PCa till it mutates into CRPC ... where as with a slow 20 month to 2 year doubling time you will almost certainly outlive it.
My SHBG started extremely high at 300, My tT was around 1000. But my bioavailable was only 84 and my free was 3.5.
I went on estrogen ADT for 5 months, and SHBG dropped to about 190, and then I started SPT.For two years I was injecting 400 mg of cypionate weekly (2 ccs of 200 mg/cc). My tT was 2200-4500+ (lab clamp). My SHBG started around 190 and steadily dropped to 80 (still dropping on BAT). I don't know why it has been dropping so much regardless of androgen therapy.
My last tT during SPT was 2245, bioavailable T was 968, free T was 36.6
I'm using Androgel so that I can take advantage of the short half-life and I dosed it down some to target tT = 1600-1800. Last week my tT during the high T phase of BAT was 1600. But my SHBG has gone down to 25-40. My bioavailable T was 1158 and my free T was 47.3.
Every few months I check vitamin D. I target 30-52 ng/ml. Last measurement was only 32 so I am increasing my D3 a little.
I only checked LH and FSH one time. I was on SPT and I wanted to see if my endogenous was zero. LH and FSH were undetectable.
I check prolactin sporadically. I take cabergoline to reduce. PRL started around 4 and is now <1 ng/ml (lab limit).
E3 was high when I did estrogen-ADT. 80-120. Not as high as I expected but my endogenous T was undetectable. On SPT it was 12-25 (I targeted 18-25 but sometimes it went lower). I measured it one time on the low phase of BAT and it was a lot higher than I would have expected (189). I was doing a low-dose estrogen patch replacement but only a 6th as much as what I used for estrogen-ADT.
I have tested DHEA a couple of times. I don't know if it is actionable. During SPT it was 83 mcg/dl. DHT was around 25 ng/dl when I was on 5ARIs and about 70-150 when off (duta had left the building but probably had some odds and ends left).
I haven't tested DHT, DHEA, LH, or FSH since I have been on BAT. I test T, E2, SHBG, D, PRL, lipids, PSA, CBC, and CMP.
LH and FSH would be interesting but not actionable. If they were zero without a GnRH drug I probably wouldn't need to mess with GnRH. But in reality I would do Lupron anyway. Seems like a good insurance policy. For some reason my T recovers very rapidly. I did 400 mg/wk of cypionate for 2 years and my endogenous T was over 250 after just a couple of months of BAT. And that included one high T cycle.
I don't know what DHEA should be. Danmeade's BAT is really simple and I'm certainly not an authority on BAT. He doesn't mess with DHEA so I don't. I do add a little estrogen in during the ADT phase though. If my T and E are both zero I lose my mind (only did that one time - never again!)
And I do add finasteride into the ADT phase. I might as well make it as ADT-like as I can.
My MO thinks that there is something to statins and metformin and a few other off-labels. I take a statin. On the ADT phase I take 500 mg or so of metformin. I'd take more but I get GI issues.
My PSA goes to 0.2-0.3 during the high T phase and zero on the low phase.
Thanks for sharing that info. Look back on my previous postings to get a flavor if my issues. It’s been exhausting. Since stopping statins my T levels are normal but my FSH & LH are persistently 2 to 3 times high blood range. No one knows why. I’ve read these are angiogenic as is PRL.
My Cholesterol rose about 25% and my T around 15 - 20% off the statin.
I’ve read the DHEA is significant for use by adrenals. Mine ran low (under 10) even on DHEA, two exception were occasions when it spiked to 650 & 215! I was able to corollate that with simultaneous use of Tgel and oral DHT.
I’ve had brain MRI. Sella was normal.
After ten years on statins, which I believe affected my T levels (cholesterol substrate to T) as when my cholesterol rose it coincided with rise in T.
My free T remains below typically around 3 even though my T now runs 500-600??!!
(nl range 6.6-18). Only exception was when on Tgel four yrs ago. And briefly before that when I I had a 6 wk trial of Clomid when it rose to 16.3.
I’ve consulted with several endos which has not been helpful.
E2 usually runs anywhere from 10-50 with several exceptions seemingly when I took Avena Sativa & DIM hoping to increase freeT (E2 rose to 209 & 170) and several times more recently seemingly connected with use of 5aRIs. (200-350 range).
After stopping ALL vitamins & supplements and 5aRIs, it is now 24.
BTW I am also on levothyroxine for Hypothyroid.
During this journey my uPSA continues a slow rise (presently 0.062).
If you have any thoughts I’d be most grateful.
My goal is to keep things as quiescent as possible for as long as possible as I am 81 this year and don’t want to face any PCa treatments including ADT.
The message I seem to get from medical SOC is when my PSA reaches certain levels, SOC can be plugged into. Frustrating but maybe such is my lot!!
I’ve learned more endocrinology that I ever cared to know and I still don’t seem to know anything!!
What is your SHBG? If tT is normal yet free T is low, then SHBG is usually high.
You might try Zytiga or Xtandi or even Casodex if your MO is inclined. For a month I did dutasteride and Casodex. I think that this combo should be good. It is rather like ADT but should be much easier to handle (my one month wasn't enough for me to get a good feel for it but Casodex doesn't carry the sides that Lupron does).
I was in love with the idea of high T so abandoned it early (my PSA was <0.01 so I'm not sure how I would have known that it was working).
Another possibility, if you don't mind taking a chance, is BAT. Your PSA is so low that I think now is the time to try experimental therapies. When your PSA is high you don't have the same margin for error.
Hi T held my PSA down to zero for about a year and a half before it started an ascent to 0.17. Then I switched to BAT. BAT has been going good for 7+ months. If BAT fails I am planning on Xtandi or radiation. Possibly a short stint of ADT to sensitize cells. Or maybe a high T pulse before or even during radiation.
I wouldn't mess around with ADT. It's a disaster IMO. I hated my 5-month estrogen-ADT bout. I didn't suffer most of the sides but enough for me to not enjoy life. I did conventional Lupron without estrogen replacement for 3 weeks as part of my BAT program. Never again! Some guys are apparently more sensitive to it than others. My wife was close to leaving me. That's how bad it was mentally. 3 weeks! I shudder when I think of years of that horror. I'd much rather die a man with my mental facilities intact.
If I were in your shoes, I would consider TRT (but consider the consequences very carefully). 500-600 is rather low. It's good for 81 but I think the optimum is considerably higher. Again, you could monitor PSA to get an idea of whether you should pull the plug on it. I was one of the rare hyper-responders. When I started super high T my PSA stayed at <0.01. Everything I read indicated that it would go sky high for a month.
FSH might stimulate growth. I tried to pin it down but found that there isn't much consensus on it. It seems more probable to me that PRL stimulates growth. Kwon at Mayo says that PRL is the #2 fuel for PCa (he holds that T is #1 - I agree but only for androgen-sensitive, AR "normal" PCa lines). Lots of research data and some studies point to Kwon being correct.
PRL is easy to control using cabergoline. I use 0.25 mg twice a week. My PRL is <1.
I haven't heard anything about LH. I'll look into it. Thanks.
I'll also look into DHEA. I tried once but as I recall wasn't very successful.
I found this about levothyroxine:
"In hypothyroid patients, SHBG concentrations increased (p < 0.01) and CBG concentrations decreased (p < 0.01) during levothyroxine treatment."
Have you had your SHBG measured? I'm guessing that it is high and that is why your free T is so low. I wonder if your LH/FSH is high because your SHBG is high so your free T is low. Then your body might be stimulating LH/FSH through GnRH activity to try to pump up the free T. Just a guess. Worth pursuing if you can find a way to lower SHBG (if you find that it truly is high). There are some ways to manipulate it but I don't know how effective they are. Mine keeps going down and if this continues I might have the opposite problem - how to increase!
It's mostly about out-of-the-box but close-to-the-box hormonal therapies. There is plenty of info about SOC therapies and in reality, the best source is your MO (for me anyway).
If you want to come up with some kind of action plan, I'd be more than happy to help if I can.
SHBG on several occasions during the last six years in mid to slightly upper mid range. BioT on several occasions has also been below range or on bottom end of normal range.
Only time free T was normal was when on Clomid (hit 16) briefly or intermittent use of Tgel years ago. Most of the time while on Tgel freeT was below normal range (3-5) but T was in 400 range and symptoms were improved so did not want to needlessly taunt the PCa. Treat the patient, not the lab data.
I may be cutting fine hairs but it appeared free T had a slight increase after stopping statin. Also Cholesterol increased along with rise in T to 500-600 range.
You can create the ADT effect without taking ADT by taking T injections or rub on cream. -- just like is done by using Estrogen patches instead of ADT. As soon as you stop the T injections your T will go to zero.... as will your PSA .. and stay there-- likely for many months...
ie. (1) Take Avadart daily at all times -- whether while on T or off T -- to knock out DHT -- the out of balance ratio of T to DHT which happens in old age -- is likely what triggers PCa in the first place... everything points to that. As we all know the facts show us that young guys rarely get PCa and almost all old guys eventually do.
(2) In your case, the day you start SPT ---( for 2 months of weekly injections 1cc T cyp (200 mg) stop all ADT permanently -- the ADT effects will linger for a few months anyway -- Then in 2 months when you stop the T injections -- Your PSA and T will drop like a rock to zero and stay there until you either start T injections again or your body starts to make T naturally again which will likely be many months.
And therein lies the problem with BAT as I see it ---
(first) the long recovery time to start making T again -- that leaves many in very low or no T for many months and induces CRPC> instead of when on the "off" ADT cycle begin immediately taking 1/3 cc (66mg) T cyp to put T back in normal range quickly... and keep taking normal range T cyp indefinitely till the PSA reaches the starting cycle and then, do it all over again.
(secondly) when the people are in the vacation mode --- when the the body finally starts back making T again it also starts making DHT again--- (5 times more potent than T --- and the body can not convert DHT to estrogen like it can with excess T) None of the Dr.'s I am aware of use Avadart -- and I think they all should for all PCa patients especially those cycling BAT.
-- just do high T for short 1 or 2 month period (shock and double strand breaks) and then no T at all for 2 months (shocks the PCa coming and going) then -- start back with normal range of T injections -- (about 66 mg T weekly or 1/3 cc T cyp) till you reach starting PSA etc etc
By the way it is almost certain that if the group on finasteride had been on Avadart the outcome would have been even more spectacular.
ADT has never been shown to cure anything but on the other hand finasteride and Avadart (which only block the ability to convert T to DHT) prevented 25% PCa and Avadart reversed 18% of post surgery/radiation PCa relapses. Other than surgery or radiation there is nothing else out there as good as that.
The only difference in Avadart and ADT is that ADT eliminated the T and Avadart does not.... and by doing so ADT causes CRPC in many cases and Avadart does not -- at least for 18 plus years and counting --- and finasteride and Avadart prevent and/or have reversed PCa in PSA relapse cases.
The recovery timeframe is variable for different men (and probably different ages in the same man?).
Here is my story:
2 years tT 2200-4500+
7 weeks ADT, tT went to zero without ADT drugs
2 weeks tT 2200 (at T0, I injected 400 mg of cypionate one time)
4 weeks ADT, tT went to zero without ADT drugs and might have started increasing at the end of the phase (might have stayed at zero, I don't know because I didn't measure it for the last few weeks of the phase).
1 weeks tT 1900-2500 (used Androgel instead of cypionate), tT did not go below 200 (as far as I know).
4 weeks tT 1800-2000 (Androgel), after stopping tT continued climbing and got to about 400. I added Firmagon (ADT drug) and it went to zero. And then BAT started working as planned.
After a while, I switched to Lupron. Probably immaterial - just easier to do and less painful.
Since then I've changed to a longer high T phase (7 weeks in my current phase). I'll see how that works soon. Meeting with my MO this week and going to start measuring PSA during the low phase which starts in about a month.
Because of the obscene variability, I do not think I can afford to go off of Lupron at this time. Maybe someday but would require intense monitoring.
If it works for you though, definitely has advantages. Unfortunately, I am a quick recoverer (too bad because I can manipulate my T however I want so don't need or want the endogenous - I wish there was a good way to shut it off outside of surgery or drugs).
So, is anyone proposing to avoid ADT when a man has chosen radiation for Gleason 4+5? The studies of RT +/- ADT are flawed for high risk PCa?Docs are knowingly ignoring a better treatment for PCa?
Your past postings regarding whether to take ADT for BCR illustrate the same problem--- prove the same point.
from your previous post: Timing of Androgen Deprivation Treatment for Men with Biochemical Recurrent Prostate Cancer in the Context of Novel Therapies
"These data provide context for patients with BCR and providers on whether to undergo ADT for years despite unproven benefit and quality of life impact. New imaging may help or further add to the controversy, since BCR patients may have metastases on newer imaging. Until definitive data are available, men with BCR should be counselled regarding the lack of data to support ADT benefit in nonmetastatic BCR."
Clearly ADT is often not helpful.... and in many cases brings on CRPC years earlier --- whereas blocking ONLY DHT with Avadart -- and not blocking testosterone has proven long term benefits --- lower PSA doubling time to over 2 years and no CRPC developing even after 18 + years of follow up... And,of those who started Avadart when BCR post surgery /radiation -- 18% had their cancer disappear.
Clearly the science is that DHT is the problem-- not Testosterone. More importantly taking away both DHT and T have adverse effects -- proven by over 70 years of little actual benefit when all is said and done.
According to the instructions for Avodart, it is said that the use of this drug for 6 months reduces the PSA level readings by 50% and then it is necessary to take this level as a control (starting). But the same instruction says that the use of Avodart does not affect the ratio of total PSA to free! In other words, during the first six months of using this drug, it is the ratio of two PSA that can be used as a marker of metabolic activity in malignant foci of the prostate! I think this is the way out!
Thank you for the interesting and useful information! It can really help me to give up Zoladex, which I dream of getting off.. Your post turned my idea of the effect of T on prostate cancer upside down.. I heard about dihydrotestosterone, but I didn't think that it was he who was the main culprit!))
It's a great thread you started! The only downside I can see from Avodart is that a small PSA rise from cancer progression, which in my case would mean from under to over 0.1, may be masked so there will be a delay getting the signal, But I suppose this is more than outweighed by the reduced risk of cancer progression in the first place.
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