I am trying to get my head round the science of ADT after castrate resistance. Why do we continue with ADT after it obviously doesn’t have any effect?? Longterm ADT has long term side effects – bones especially.
And if intermittent ADT (100% dose til psa rise) is non inferior to continuous ADT - can we make a version where the ADT standard dose is taken but at double the interval – which means giving a shot of ADT at regular intervals to prevent progression rather than waiting for progression and then going back on a full dose as in IADT. Can this maintain some level of ADT, but not as severe and the T level will remain low?
Does the idea of moderate doses give way to the possibility of a longer time to regression?
Can all you knowledgeable guys out there throw some light on this???
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Stoneartist
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Even when you are castrate resistant only part of the tumor cells are resistant. You continue with ADT to control the cells which are not resistant.
The side effects are caused by the low T level. If you get another shot of ADT while your testosterone did not fully recover the side effects will continue. If Lupron would not lower testosterone it would not cause side effects.
Most of the side effects can be mitigated with estradiol patches.
I’m sure there is much variation as with everything. Hot flushes and mood swings seem to be reliably and completely resolved. Fatigue and mental fog seem partially improved to me, about 50%. Bones get stronger but muscles and response to exercise not.
Does anyone know if estradiol patches interfere in any way with the effectiveness of Firmagon? My scans are all negative and my testosterone and PSA are undetectable so I guess the stuff is working. I just feel like a piece of garbage, especially on the golf course.
Prostate cancer cells need testosterone, not estrogen. Therefore the patches will not decrease the effectiveness of Firmagon. Muscle loss is caused by the lack of testosterone.
Estradiol reduces bone loss , joint pain and cardio problems; of course it also stops hot flashes but only one patch is needed for that. It does not imho reduce fatigue. Weight training helps with that issue. Bob
I learned something today on the golf course. Temperature was 70 with low humidity. I never had one hot flash and had much more energy than those days when it's 85 and humid.
That makes sense doesn’t it? I’m turning 78 and have been dealing with this since Dx in July 2013 at age 69. Awhile back I developed neuropathy in feet which screws with balance which is so important in golf and I’ve lost 30-50 yards. Golf is not fun anymore.
Stand a little wider and flex your knees a bit more for balance. The balance problem is probably on your follow trough so play the ball a little farther back in your stance so you won't have to make as strong a weight shift through impact as you would if the ball was more forward in your stance. Finally, play the front tees. That's what I do sometimes. It's more fun.
I am 76 and 31 months on ADT. Two years ago I was driving 230 yds. Now I am getting 210 yds. I am finding it more difficulty with my irons especially getting carry to drop the ball on the greens. We have all table top greens. I suspect at least 15 to 20% drop in distance.
Stone artist...You asked one of the most important question one can ask about Prostate cancer and its treatment.In the beginning, Every PCa tumor has 3 different types of cancer cells..(1) Fully androgen sensitive (2) Partially Androgen sensitive and (3) Androgen resistant.
In man A, first type cancer cells may be 99%, second type cancer cells may be 0.7% and third type of cancer cells may be only 0.3%.
In man B, the ratio of these 3 type of cancer cells may be 75%, 10% and 15% at the outset.
So , how the initial ADT will work on these 2 men ? In man A.. just Lupron alone will kill 99% of cancer cells. In Man B, only 75% of of cancer cells will be killed by plain Lupron.
So...How do I find out ..if I am like man A or like Man B ? There is no direct test to know this.
Indirectly, we can estimate . If your PSA falls down to a very low level after initial ADT.. say 99.5% then, you can assume that almost 99.5% of your cancer cells are fully Androgen Sensitive (at least in the beginning) Also, if your total Testosterone plunges below 10 ng/dl it also indicates very good outcome.
how long these mentioned 2 men are likely to live ? Clearly.. man A will likely to live much longer than man B. Studies show that men like man A are likely to live 6 to 12 years in comparison to men like man B who can expect to live about 3 to 5 years (with more intensive treatments)
Coming to later part of your question...If cancer cells are suppressed heavily and continuously in man A type men...the androgen sensitive cells will find a way to become androgen resistant and that is why it is said that men will become castration resistant in 2 to 3 years...This is a bad generalization... it is very individual phenomenon.
The danger of SOC directive is that they assume all men with PCa are like man B...and that ends up in unnecessary overtreatment of man who are like man A. So, lot of men like man A will become castrate resistant much sooner than they would have...if they were treated with milder, less intensive treatment. Man like man A can safely go for Intermittent ADT with close monitoring of biomarkers and will delay castration resistance and prolong survival.
This is called 'individualized, precision treatment" ..but SOC lumps every man as "aggressive cancer" and dumps all treatments at once on every man...Certainly it does increase their revenue ..but is it in best interest of individuals? ...I do not think it is.
Your explanation of person-specific adrogen sensitivity was very helpful to me. Thank you. I have a couple of questions, in case you or others know something or even have guesses.
1. Does Gleason level indicate, in any way more, more or less liklihood of adrogen sensitivity?
2. Would a biopsy of a metastasized lymph node help identify likely adrogen sensitivity within the cells?
3. Does the PC medical world need a new measurement, like PSA and Gleason, to identify adrogen sensitivity (like maybe AS )?
I’m my experience, having been diagnosed in July 2013 the aggressiveness and volume of the Pca dictates the survival rate . And of course the aggressiveness of the treatment . I have low volume but aggressive Gleason 9 Pca so my Mets are defined as oligometastatic and treatable with radiation and ADT. I switched to estradiol patches from trelstar over three years ago . I’ve never seen a MO but will next week as my psa is now at .8 . A recent dcfpyl psma ct pet scan didn’t find much to worry about.
Good info. Do have a reference that a total T of less than 10 implies a good outcome in metastatic PC. I have stage 4 mPC. PSA in 3 mo from2250 plunged to undetectable for 2 an 1/2 years. Total T down to <1 after 2 mo of ADT. Thanks.
Excellent results. Your Nadir PSA is undetectable (as good as it can get) and Your Nadir T is <1...and to top it all.. your Time To Nadir (TTN) is over 12 months. So based on these findings, you have very very good prognosis...based on studies, you come in category 1 which predicts median survival of 78 months. (note it is median wwhich means 50% people live longer than 78 months)
I have a copy of the study in one of my files. You can go to pubmed and search "nadir testosterone" by author Lawrence Klotz. And an Older study by Maha Hussain about Nadir PSA and survival.
Skipper, Person-specific analysis and individualized ,tailormade treatment is the future of PCa treatment. We talking these concepts way ahead of current "one size fits all" mass treatment where a protocol is designed and shoved in every patients throat.
(1) Gleason grade tells us about degree of deformity and distortion in cancer cells...means it tells us how different cancer cells have become from normal cells. Gleason grade 3+3=6 is almost 99.5% like normal cells whereas Gleason 5+5=10 is only 10 to 15 % like normal cells. in this way , Gleason 3+3 is almost like a normal law abiding citizen who once in a while steals a beer or 2 from a grocery store. In contrast, Gleason 5+5 are like hardened criminals who left their regular job and indulge in full time robbery, burglary and other criminal acts.
In simple way.. Gleason indicates degree of INVASIVENESS of these cells...higher Gleason.. means meaner and violent cells who create havoc . These are bad a*ss cancer cells.
So, Gleason 5+5 are going to invade and move fast by multiplying and forming colonies in bones and organs.. they have much high level of criminal skills than poor Gleason 3+3 or 3+4.
(2) Biopsy of cancer cells will only tell morphological features and shape etc...it can not tell physiological functioning of these cells.. thus...Biopsy can not tell degree of androgen sensitivity.
(3) Yes...the researchers need to find out various biomarkers and other tests to estimate degree and percentage of fully androgen sensitive cells so precise, targeted treatments can be designed for every individual. But.. who is interested in this...may be just you and me whose lives are on line.
My biopsy showed Gleason 3 + 4 =7......... when the pathology was done after RP, it showed about 1/3 of the cells were Gleason pattern 5. Not sure what my real Gleason number should have been, but clearly it was not 7
"Real" Gleason Score is based on the highest, worse, number, not an average or adjusted by lower numbers found in other areas. Kind of like if you have an accident and break a leg and sprain your other ankle. The broken is what get treated. G 3+4 is much better than 4+3.
I better understand now. I would ask an Oncologist, NOT urologist, what they think your score should be. You need to have your biopsy results in your hand when you do. Also try for a female oncologist as they are much more empathetic and understanding of you. Hoping for the best for you and please let me know how it goes. I am now on Nubeqa and starting my 7th year from diagnosis. G9 initial and radiation including Brachy boost.
I am actuaully in my 5th year since RP, just never had the onc or uro tell me what my "real" score was..... guess it doesnt really matter, all I need to know is its aggressive. I am also experimenting with Nubeqa, altho i am going against standard of care. I had pretty bad side effects after almost 3 years of continuous ADT that got really bad when we added Xtandi. I am now experimenting with nubega as a monotherapy..... so far so good, but PSA is creeping up.
After RP you get a report about the operation or you can ask for it. It will tell you your actual Gleason score after the prostate is biopsied slice by slice.
I got one of those, it describes how much grade 3, 4, and 5 cells are present, but no mention of a Gleason score..... I think they may be phasing out the Gleason system
Back when I was diagnosed, the term "castrate resistant" wasn't used. It was thought that the cancer no longer needed androgen. Terms such as "androgen-insensitive" or "hormone refractory" were used. The PC3 cell line, obtained from a bone met, was thus described and was used in thousands of studies as a stand-in for all bone mets.
But then it was discovered that in cells that become resistant to classic ADT, the androgen receptor [AR] generally remains in play. That led to the development of Abiraterone, etc.
While it may seem that ADT has failed, the "AD" part is working fine as long as testosterone is <20 ng/dL. If one's post-ADT therapy targets the AR-axis - & that includes the "lutamides" - classic ADT is usually continued.
Agree ..Targeting AR axis is the way all Lutamides act. They block AR (androgen receptor ) at local level...so technically Lutamides are not ADT. Androgen deprivation is accomplished by all Lupron type meds and Abiraterone does the same thing..i.e. Androgen deprivation..by blocking the enzyme CYP17A and closing all three sites of androgen production. So when Abiraterone is added to lupron..it works like "ADT Booster" and can destroy partially Androgen sensitive part of tumor.
Lutamide does not lower Testo. ..lupron and Abiraterone does lower Testo.
PatrickSo given that I’m on only estradiol patches , psa has risen over 2 3/4 years from nil to .7, T is around 3 and E2 is between 150 and 200, what and what point would I need to change my hormone therapy cocktail ?
Also I’ve been having pain in left clavicle which would normally be a signal for a scan since I’ve had three bone Mets in the past (1 in 2017 in femur) and 2 in 2018 ( one in clavicle and one in a rib) which I treated with SBRT . I’ve never had pain from previous bone mets so this may not be a met. I suppose a normal mri is indicated first? To find the previous three I used axumin on the femur and psma ct pet on the other two.
It DOE@@@ have an effect. Even a bigger effect than it ever had before. One of the primary reasons for castration resistance is "amplification" of the androgen receptor (AR). This means that each cancer cell makes many more copies of the AR on the cell surface. When that happens, the cell is activated to replicate with even the smallest amount of testosterone.
Unfortunately, castration resistance comes at the same time whether you are on intermittent or continuous ADT. Only more powerful AR-directed medicines and cytotoxic agents slow progression.
This is very interesting information - and many thanks to you all for such clear descriptions of whats going on. My takeaways are
1. its the low T that gives the side effects not the drug (I am on zoladex every 3 months and mt T is 0.0 Nmol/L) so it wont make any difference if I take one Zoladex shot every three months as prescribed, or if I skip alternate shots giving one 10mg shot every 6 months.
2. Its important to keep the T level low because there will still be some cancer cells in there which are androgen sensitive - whilst others have developed castrate resistance.
3. So we flood the expanding AR points with Xtandi (or other similar AR directed stuff) so theres nothing available for the cancer cells to feed on.
Seems to me therefore that as long as T is below castrate levels then ADT shots are less important - hence no difference between ADT and IADT - and as long as it is the low T which gives the side effects there is no real benefit from cutting out ADT
2. is only partly correct. ALL prostate cancer cells remain sensitive to androgen stimulation. It is just that they can replicate even without external androgens (via internal androgen synthesis, internalizing the AR, using other ligands for activation, etc.). External androgens make it easier for them to replicate.
3. works for some time but not forever. Cancer cells internalize the AR and are activated by other ligands that Xtandi doesn't block. Cancer cells react to blocked ARs (with anti-androgens) by creating even more ARs. It's a feedback loop.
Getting T below 20 ng/dL has been found to be more effective than getting T below 50 ng/dL. The AR becomes exquisitely sensitive to even the slightest amount of T. Getting T down as low as possible is an even bigger benefit when one is castrate-resistant
Can I also put my five cents in the general piggy bank of knowledge from personal experience ..)) Many comments are correct, but there are some points that need to be distinguished in order to understand what hormone therapy is! Hormonal drugs are divided into three types: 1. LGRG agonists (Leuprorelin, Goserelin and others) 2. LGRG antagonists (FDA approved only Degarelix) 3. Antiandrogens (Flutamide, Bicalutamide, Nilutamide, Enzalutamide, Abiraterone and others). The first two groups of drugs do not affect prostate cancer cells in any way and only turn off the Testosterone production line in our pituitary gland! Thus, there can be no resistance in cancer cells to these two types of drugs! These drugs belong to the group of drugs of medicinal (chemical) castration, which is equivalent in effect to physical castration. The third type of hormonal drugs, antiandrogens, is used as an addition to the first type of drugs, LGRG agonists, to achieve maximum androgen blockade. Antiandrogens affect the androgen receptors of prostate cancer cells and prevent androgens from binding to them, and thereby preventing the conversion of testosterone into dihydrotestosterone, which all prostate cells feed on, only cancer cells consume it 200 times more! It is precisely to the drugs of the antiandrogen group that resistance arises over time in these cancer cells, which requires switching to the next drug from the antiandrogen group! Drugs of the second type of LGRG antagonists do not require the addition of antiandrogens to the treatment regimen, they have twice as many side effects on the cardiovascular system and to date, all studies have proven their advantage over LGRG agonists, but at the same time they have a pronounced allergic syndrome at the injection site! I personally have experience using both Degarelix and Goserelin. The first drug did not suit me precisely because of the allergy at the injection site and it was difficult to put on underwear and trousers ..)) Since 2016, I have been using the drug Zoladex 3.6 mg, which is confirmed better than depot 10.8 mg keeps Testosterone at 0.087 nmol/l constantly.. I think this is due to the uneven release of the drug from the depot for a longer period of time (3 months at the depot of 10.8 mg). Experimentally, adding 5 days each time, I achieved the frequency of administration of this drug once every 45 days, the Testosterone level is still 0.087 ng/ml! For the duration of the therapy according to the experimental protocol "177Lu + 225Ac - PSMA-617", I suspended my experiment so as not to interfere with the treatment, but I think I will continue and bring this period to 60 days calmly! I think that manufacturers deliberately shorten these terms and overestimate the dosage of medicinal products in order to have maximum profit! Thus, numerous studies have already proven that taking Abiraterone at a dose of 1000 mg on an empty stomach does not change the therapeutic efficacy when taking Abiraterone at a dose of 250 mg together with a light breakfast.. But the side effects in the second case will be 4 times less! Conclusions, as always - everyone does it himself!)) And I apologize for such a long comment! And finally, I want to recall the words of Professor of urology Bertrand Tombal: "The appointment of ADT drugs depends on the personal characteristics of the urologist (education, place of work, etc.), and not on the condition of the patient himself!"
The dynamics of my PSA and Testosterone. Now the PSA is 0.140 ng/ml.
Great comment Rusland - and I am especially interested in your comment about prescribing max dosage - as I am looking to decrease my dose of Xtandi from 160mg to 120mg - working on evidence that this will maintain the same concentration. Many thanks
Actually it was only when I saw that the text on the excel diagram was in russian that I realised that you were russian - so the translator did a fine job!!
Only translation mistake was switching nM/L to ng/dl for T values.Only conceptual point In my opinion is grouping abiraterone with the lutamides, as is commonly done. Since it powerfully blocks testosterone synthesis rather than acting at the AR directly, it is more appropriate to group it as a more powerful form of ADT. It may not need LHRH drug to achieve castrate testosterone levels as some have seen. It was just tested as an add on to ADT in trials so that is how it is typically prescribed.
There is no error with nmol / l, it is in these units that Testosterone is measured in Russia! But according to your comment, I saw an error of the translator from Russian to English.. LHRH translator translated as LGRG...)) Thank you!
Your first level was in nm/l. Then later you wrote it was the same level numerically in ng/dl. No big deal. Just that you asked. We all put up with auto-correct frustration, but we can understand regardless. Brings some humor in. Cheers! 😆🤔👍
Yes , here it is quite obvious my mechanical error when using units of measurement for PSA and Testosterone .. - just like you, you read Testosterone and intuitively imagine ng/ dl, although I have ng/ml written ...)) And I absolutely agree with you that humor is our everything, without which we would have been in the next world for a long time!)) God grant us more, as long as possible to laugh in this world! 100%
It may be worth going on the other side, as I did, to try to reduce not the dose of the drug, but the period between taking Enzalutamide 160 mg more than once a day (24 hours), gradually increasing the interval by 4 hours for three days. For example, this morning at 8.00 you took 160 mg, the next day you take the same dose at 12.00 o'clock, on the third day the same dose, but already at 16.00 So for three days you take the drug once every 28 hours! And so gradually and carefully increase the intake interval of 160 mg once every 48 hours.. Because I'm afraid that reducing the dose of the drug itself will very quickly lead to resistance to this antiandrogen! This is approximately like an antibiotic, the dose of which cannot be reduced in subsequent receptions, you can only reduce or increase the number of days of admission!
It should be understood that Enzalutamide belongs to the third group of hormonal drugs in my first comment, which affects the receptors of cancer cells and reducing the dosage is likely to lead to resistance of these cells to this drug! But the increase in the time between taking the same dose is possible to experiment, but control the PSA at the same time!
This is all very interesting. Wednesday I have an appointment at Dana Farber. The test trial has two groups randomized. Group A (Enzalutamide) Group B (Lu PSMA 617).
Unfortunately, I do not know who Dana Farber is..(( If this is the head of the test trials, then tell her by any available means or at a personal meeting that the results of such an experiment will not be reliable if the status of patients on FDG is not determined before the application of 177Lu - PSMA-617! To do this, it is necessary to conduct a PET-CT study with the drug 18F - FDG! I have sufficient statistics in this regard about patients with prostate cancer, whom I helped to get treated under this protocol with the isotope of Lutetium.. Approximately 50% of patients have a positive status for FDG in this case, the expected therapeutic effectiveness of the use of Lutetium is sharply reduced to zero effect! As a rule, in all medical nuclear centers of excellence with FDG(+) patients, more than 50% of malignant foci in therapy with the targeted carrier PSMA-617 are denied! I can explain to Dana Farber the reason for this phenomenon myself, or try to arrange for her to contact the head of the nuclear center where I myself was treated with Lutetium and Actinium isotopes! My email: abubakirov66@gmail.com
A patient with prostate cancer FDG (+) more than 50%. He was denied Lutetium treatment!
Yes, PET-CT with the drug 68Ga - PSMA-11 is a prerequisite for determining the status to PSMA.. I was talking about an additional PET-CT study with the drug 18F - FDG.. These are two completely different studies!
Sometimes a protocol is chosen that if the FDG avid sites correspond to the same locations as PSMA avidity. This is called concordant, and Lu /+-Ac PSMA may still be pursued in that there is a (short) range of targeting of other cells around the PSMA avid cells. If there is discordance between the two scans then of course it is futile.
Absolutely right! Cells in malignant foci eventually mutate from PSMA receptor cells into NE cells that do not attract PSMA carriers loaded with therapeutic isotopes, but due to the radius of action of the same isotope of Lutetium (2mm), they are able to attach to the part of cells that have PSMA receptors and destroy those cells that do not have such receptors! But when PSMA receptor cells in the tumor become less than 50% - all therapy with PSMA carriers is reduced to almost zero! Unfortunately!
My doctor lowered mine to 120 so casualy and there was no change in lab results. I see that some are on 80, but will wait and see. All this conservation will require more study for me to comprehend.
I have already written above that experiments with lowering the dose are undesirable if your cancer cells have already met with a dose of 160 mg! As it can lead to rapid resistance to this drug personally in your case.. Now, if a dose of 120 mg was initially administered, this is another matter, then perhaps it will cope as well as a dose of 160 mg.. Personally, if my cells are already familiar with the 160 mg dose, I would try experimenting with increasing the time between injections of the drug!
I took Xtandi at a dose of 160 mg, but did not conduct experiments with it because I trusted my doctor and it was a long time ago.. And by the way, it was enough for me for only 7 months before the onset of complete resistance, and after this drug I already switched to Zitiga.. I did an experiment with LHRH, specifically with the drug Zoladex ® 3.6 mg. I gradually increased the interval between injections starting from 30 days plus 5 days after each application.. Before each subsequent injection, I measured my Testosterone level and brought the frequency of taking this drug to once every 45 days without any damage to my Testosterone level! It was also 0.087 nmol/l, as in the case when I injected Zoladex 3.6 mg. once every 30 days.. I have completed therapy with 177Lu + 225Ac and now I intend to continue my experiment with this drug bringing the interval between injections to 60 days! God bless us!
I agree with what RusLand is saying.. about starting at low dose and later go to high dose if needed.I started with 50 mg a day Bicalutamide monotherapy and that kept me fine for about 8 months and then, PSA started creeping up so I went up to 100 mg Bicalutamide a day which worked for another 6 months. And, then I increased dose to 150 mg a day, got 2 months more . Thats when I stopped Bicalutamide. But I enjoyed good quality of life for 16 months using this approach. Almost no side effects. Then went for Abiraterone Monotherapy on Sept15,2021. My last Lupron (or any Agonist med) was more than 2 years ago. Currently doing ADAPTIVE intermittent ADT with PSA 4.0 at lower set point and PSA 10 as upper set point. I will report on this once I achieve a year on this therapy. But men have to first know their prostate cancer very well before embarking on such experimental treatment strategy.. I figured out early on that I am like Man A described above.
Overdosing is as big a problem as underdosing. But our fear makes us weak and vulnerable to accept any treatment thrown at us.
Good info. I am 2 months into Xtandi using 120 and 160 on alternate days. T in 0.0 and PSA less than 1.0 on the way down, time to castrate resistance on Zoladex was 21 months (Nadir PSA1.3). Next blood sample in 3 days - so Im gonna fish out that info - Thanks
You don’t include Estradiol as ADT. Why is that? Because it reduces T by increasing estrogen? Estradiol has way fewer side effects than any of the SOC first line ADT meds but it does cause man boobs and fatigue. But. I suppose the fatigue is caused by low T not the estradiol correct?
Is it possible that I don't know something..?! But in Russia estradiol is used in relation to men only in three cases: 1. Breast cancer in men. 2. Palliative care (anesthesia) in hospices for castrate-resistant prostate cancer. 3. When a man wants to become a woman. No laboratory tests for prostate cancer for the level of estradiol are required from us, except for T.. I'm sorry!
Of course, this is very interesting information! But I understand that this study conducted in 2014 has remained just another study.. Because I have not met approved protocols for the treatment of prostate cancer with the use of subcutaneous administration of estradiol! I have also not met estradiol preparations for subcutaneous administration! Maybe I don't know something and missed the FDA approval for this drug? But when I read that this is a cheap alternative to expensive LHRH, I immediately imagined the faces of the manufacturers of this LHRH ..)) I think that says it all!
Where does NUBEQA® (darolutamide) enter into your listing? I am on my 7th month with this and monthly Lupron. PSA is now <0.02ng/ml and testosterone is <5ng/dl.
The drug NUBEQA ® is an antiandrogen! Therefore, it is included in the third group of hormonal drugs such as "Flutamide, Bicalutamide, Nilutamide, Enzalutamide, Abiraterone and others" Thank you!
I went all the way through hormone therapy and sooner or later I developed resistance to all hormonal drugs since 2016! The only drug from the LHRH agonist group is Gozerelin, which keeps my T at the castration level and I am blogged to it! Next, I am already being treated in parallel with PSMA, which destroys my cancer cells with the help of Lutetium and Actinium isotopes.. I have been living and fighting with this creature since 2016 and this is the most important thing!
Yes, yes.. I will learn here the secrets of the treatment of prostate cancer in Americans and talk about them in the KGB ..))) One very important secret I have already learned is good humor! 100%
Thats an interesting approach. So far I have calculated the steady state values for three doses and we can see on the curve that without any other factors than we should reach "saturation " using 160mg/ day after about 9 days, but that 120mg/day will still maintain saturation levels once they have been reached, whereas 80mg/ day looks like it will flatten out at just under saturation level. But this in over simplified since saturation level may vary with dose, and there may be other factors which should be taken on board - its a bit tricky finding the correct scientific details - but the idea is still there - use i60mg to get up to saturation - and a lesser dose - with lesser side effects to maintain saturation. - a bit like accelerating a car and then maintaining cruising speed.
Very interesting thread from your question, Stoneartist. One aspect of the “equation” not mentioned is the “bimodal” response of PC growth to testosterone levels. This is the basis for BAT and has been discussed in other threads. Certainly PC is powerfully suppressed in growth when T levels are castrate (<20 ng/dl) until very advanced. However, high to very high testosterone levels also can also suppress, rather than stimulate PC growth, though not for everyone. Rather it is relatively low but not castrate levels of testosterone that most strongly stimulate PC progression. So it appears better to either have castrate very low levels or high levels, high normal to Supra normal. And don’t mess with Mr. in-between. That is the problem with IADT “vacations”. Testosterone often recovers only partially for a long time. So, not only does one not enjoy the benefits of testosterone recovery, but it may not be beneficial in the long run. I wonder if perhaps this is why IADT has not been shown to be superior to continuous, rather than just non-inferior.Disclaimer: I am on modified BAT program cycling between Supra physiologic T levels and castrate levels.
My 2 cents here , i missed my Lupron injection planned around the onset of COVID. The urologist i get it from was not scheduling. I had been on ADT for 10 years and Xtandi now, for over 2 years.
I always questioned why i needed to stay on Lupron, since it failed and i was told there may be some cells its taking care of.
Well, missing the lupron i felt so much better after 9 months or so i didnt want to go back on, naturally. I figured my body was wrecked enough that i wouldnt produce much testosterone. Well i was right, im still castrate but PSA is creeping up ever so slowly. Last check i was.029. I was also informed many times that a man with his prostate, anything less than 1 is pretty much zero.
Now i am told i need to get Lupron now. I asked my urologist why. All he could muster up was its American urological Association protocol. Lupron for life . My Oncologist , after prodding said i will have trouble getting any future medication paid for if i dont take the lupron. So there you have it, i feel its mainly a money thing. You can make your own conclusion and ask your own questions. I do not trust Pharma or soctors that just cite protocol. Im different than everyone else as you are too. I can read lab reports just as well as they can.
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Castration Resistant?
Castration Resistance
Does Intermittent ADT delay castrate resistance?
