By now, most will know that ADT as monotherapy is not immunosuppressive. Testosterone [T] at normal-high levels is immunosuppressive. To that extent, those who had high T before ADT will have removed a risk factor. I don't know how low T has to go before we can ignore it as a risk factor. 350 ng/dL is the cutoff for hypogonadism. Many men are near this level at diagnosis. I doubt that ADT would confer much if any benefit to those men.
But now a new problem has raised its head. As most will know, men with PCa (as a group) have higher cardiovascular disease risk. In fact, in some vlog psts, Dr. Myers seemed more concerned about keeping patients from dying of CVD than PCa.
Well, it turns out that COVID-19 attacks the heart in 20% of patients in the general population. Could be higher in this group. Some patients present only with heart issues & lungs are clear. It's a scary idea that one might be entirely symptom-free yet have one's heart on the verge of giving out.
Ironically, a strong immune response to COVID-19 & the resulting high level of inflammation might contribute to a cytokine storm & heart damage. (Bring back my T. LOL) Those who are already managing inflammation may fare better.
There are situations where one does not want a robust immune response. Although one can say that COVID-19 causes heart damage in some, it may be the strength of the immune response that causes the damage.
See:
[1] JAMA yesterday.
"The Chinese Center for Disease Control and Prevention recently published the largest case series to date of COVID-19 in mainland China; the overall case fatality rate was 2.3% (1023 deaths among 44 672 confirmed cases), but the mortality reached 10.5% in patients with underlying CVD."
[2] Science Daily.
[3] New York Times.
"The study, led by Dr. Zhibing Lu at Zhongnan Hospital of Wuhan University, found that 20 percent of patients hospitalized with Covid-19, the illness caused by the coronavirus, had some evidence of heart damage.
"Many were not known to have underlying heart disease. But they often had abnormal electrocardiograms, like the patient in Brooklyn, in addition to elevated troponin levels, which sometimes soared to levels seen in patients with heart attacks.
"The risk of death was more than four times higher among these patients, compared with patients without heart complications."
Referring to the Italian case in [4]:
"... describing a previously healthy 53-year-old woman who developed myocarditis."
"... her electrocardiogram was abnormal, and she had high levels of troponin in her blood. Because of the coronavirus outbreak in Italy, doctors thought to test her and found she was infected."
"Dr. Enrico Ammirati, an expert in myocarditis at Niguarda Hospital in Milan who consulted on the case, said the patient’s heart problems were likely caused by her body’s immune response to the virus."
[4] Italian case [Jama]
***
Note that: "The cardiac subtype of troponin T {TnT} ... is released into the blood-stream when damage to heart muscle occurs." [5]
Why does T "before" ADT remove the immunity risk? So if you do high T and then start ADT your immunosuppressive risk is decreased? Note: I did ADT early last year (after G4+5 diagnosis and RP). But since Sept 2019 I've been injecting 400mg of testosterone cyp a week (ultrasensitive PSA is zero and inflammation markers are low).
Trust but verify. In other words, do not trust... American SOC is rather lame also. That said, one of my doctors is SOC and she's very sharp and I trust that she is telling me what she believes to be true and not an uninformed SOC line. I respect that.
Not trying to hijack this thread, but I was on TRT (TestC 200mg/week) before being diagnosed with PCa in October 2019. My urologist at UCLA said I should temporarily stop until I get my treatment figured out, which I did. I had HDR Brachytherapy in February 2020. My RO at UCLA said I should wait 6 months before starting TRT. The Medical Oncologist I saw at Prostate Oncology Specialists recommended starting TRT right after my procedure.
I want to get back on TRT and would be interested in your in your archive of protocols for TRT users.
Low systemic inflammation not only controls PCa growth but also prevent cytokine storm and heart damage.
We need to keep taking our anti inflammatory food, herbs and spices such as turmeric, ginger, garlic, quercetin etc to keep our C reactive protein /inflammation as low as possible.
To prevent heart problem, This way, we can mitigate three higher risk factors in Covid19 situation ..
I have heard that just a small amount of black pepper makes the curcumin in turmeric far more bioavailable, so I always add a grind or two.
A common way to use those three (plus pepper) all together is in any simple curry dish, or as part of the the spice base for a simple red sauce. If you are not especially fond of turmeric flavor, it is a lot less pronounced when buried in tomato, olive oil and oregano!
I forgot to mention that I was also using Arimidex (anastrozole) 1mg EOD to get my estradiol between 15-20 and my T was around 1000. Yes 400mg is a cycle, but to each their own!
It seems to me that being on any treatment (or not) that is immunosuppressive (or not) may not necessarily determine the nature of your immune response to COVID. But it sure looks like being heart-healthier, lung-healthier and having less severe (or no!) diabetes or metabolic syndrome gives you better odds.
This is from a few weeks ago:
“These people are dying of an inflammatory process in their lungs. It’s not an infectious process, like a bacterial or viral infection. It’s inflammatory, like we see with SARS,” that drove some people’s immune systems into overdrive, leading to cytokine storm.
Immune response seems to be worse in people with underlying health conditions, the Chinese data showed. Aylward said, “the proportion of people who die who had cancer was half compared to hypertension and cardiovascular disease. Diabetes is a little bit lower than those two, and cancer lower again.”
-Bruce Aylward, who led the WHO mission to China
In Italy, many of the dead have three or more preexisting conditions. The most common was hypertension, followed by ischemic heart disease and diabetes.
It may be a little late to really "get healthy" in time for the impending peak infection a few weeks away, but we should remember there is no guarantee that the decline of COVID-19 means we are safe from COVID-20.
No problem. I like answering questions (and asking them
In 2018 I had an RP at Mayo. Gleason 4+5. One lymph node. Seminal vessels and bladder neck involvement. Mayo oncologist and urologist "guaranteed" me that my PSA would go up within 3 months and the cancer would return. They said that I would have to do radiation in 2019 and follow with Chemo.
Instead I did IV-C (50g-100g 3x a week) and 3-6 grams of curcumin a day. I also started eating a plant based diet. My PSAs were zero through 5/2019 when I started estrogen therapy to reduce my T (I don't know if I would do estrogen therapy again - perhaps high T injections with a testosterone that has a short half life - or perhaps even an oral, that would likely cause my body to stop making endogenous T. Then cycle off. T would hopefully go castrate. Then back on (pretty much a BAT routine but no Lupron).
Or I would just do what I'm doing today. For about 7 months I've been injecting 400mg cyp a week. And taking an AI (letrozole [a very low dose of 0.6 mg a week] is the only main one that is effective for me - no bloating). Also I take finasteride 5mg and dutasteride .5mg daily. I just added cabergoline
0.25mg 2x/wk to reduce prolactin. I have a baseline but won't have an idea how much to take until I get prolactin measured again.
T range is between 2380 and 2850
DHT is 50 (seems like it should be lower)
Estradiol is lowered very effectively by letrozole and was undetectable. So I cut the AI from 1.2mg a week to 0.6mg a week and now estradiol is about 15.
Prolactin is 9.1 but this is a baseline BEFORE starting the cabergoline.
I also take metformin and a statin (mostly red rice yeast but I also take pravastatin). And thymosin alpha for WBC count. Seems rather effective - increase in count was about 20% for first month. I'm still working on dosing. I suspect that, even though it has a short half life, a large dose followed by a decay to zero might cause the body to produce more WBCs and natural killer cells. I have a hemocue WBC analzyer and I measure the WBC count a few times a week. So I should have an idea about dosing and timing in a month or so.
Sort of my own protocol but similar to Friedman and Dr. Bob. I see Dr. Eshaghian at Compassionate Oncology. He said that "you are firing lots of SCUD missiles at the cancer but we have nuclear bombs." I'm going to continue with the SCUDs since his nuclear bomb involves Lupron for 13 months with low dose chemo.
But most of the stuff that I arrived at through research is identical to their stuff. With the exception that I stress weightlifting, exercise, diet, and fat loss while they do not. I also think that there might be a metabolic aspect but they do not seem to be on the same page. And Dr. Eshaghian did not think that estrogen had anything to do with my T being undetectable during my estrogen therapy. I might be wrong but he didn't seem to have a theory. Odd since I provided him the lab results and the mechanisms are clear to me. Strange how many trained doctors don't seem to quite understand how the body regulates T in response to exogenous E.
I have noticed that many of the NIH therapies that seem to be effective are ones that increase muscle mass and decrease fat. I feel great and, despite lots of weightlifting throughout my life, am in the best shape I've been in since my 30's. Wife loves it too.
in reply to
Also, although I was warned many times not to even look at my PSA when I started T, it stayed at zero for the first couple of months (yes I looked ). Then went up to 0.04-0.06 and now is back to zero (<0.04).
PSA is not actually specific to the prostate and a small amount is made by other tissues. So there is a remote but non-zero possibility that the Mayo urologist got all of the PrC removed. And I don't want to push my beliefs on others, but I hope that God did not have it in his plan to remove me from the world this particular way. In which case everything that I, or the doctors, do or do not do is immaterial.
It does seem the DHT is high given the use of finasteride and dutasteride. But I wonder if it is because your T is so high. I think it's all relative.
I just take dutasteride every other day and my DHT < 5. T is 800+ (no supplemental T). My E2 is low 30s, but I don't take an AI. My naturopathic oncologists says the E2 is perfectly in line with the T, which makes me think they are looking at relative numbers as well as absolute.
Question - why did you start the estrogen or go to the BAT routine if your PSA was zero... or did I read that wrong and it started to increase after 5/2019?
And, always nice to read about individual protocols that are working. Congratulations on your success and thanks.
"naturopathic oncologists says the E2 is perfectly in line with the T"
I too think that the E2:T ratio is more useful than E2 or T alone. If it was me, I'd still try to get E2 below 30. Many years ago I used chrysin & piperine, which was very effective. Now I use Arimidex.
Thanks. I couldn't stand ADT (muscle wasting and no libido). I started researching testosterone and estrogen. It appeared to me that testosterone at a supraphysiologic dose might kill PrC cells. But only if estradiol is kept low. Then I found work by Dr. Friedman and Dr. Liebowitz. They echoed what I thought and expanded upon it - also added real case studies.
I think that the reason why it was concluded 80 years ago that testosterone causes PrC was that estradiol wasn't kept in check (no AI's existed so they couldn't control it). Even today most experiments on testosterone do not involve estradiol control. And the NIH did some population studies and there is an inverse relationship between testosterone and PrC! They even adjusted for age and found the same thing. So, as far as I know, it has not been proven that testosterone exacerbates PrC. Could be anything that is changed by exogenous testosterone. Estradiol, DHT, prolactin, ?
However, if my PSA increases and doesn't stabilize I'll likely change my approach. PrC is heterogenous and my current thought is that testosterone only kills some of the population. Perhaps DHT actually kills some. And maybe taking away t and e also kills a subset. And perhaps estradiol by itself with low T kills a subset...
If this is true a BAT type approach might be the way to go (with some tinkering with DHT and E).
You say "I think that the reason why it was concluded 80 years ago that testosterone causes PrC was that estradiol wasn't kept in check."
Actually, I'm not even sure everybody reached that conclusion! What they discovered was that the removal of T caused a (temporary) remission, so some people simply assumed the inverse: if removing T stalls PC, then adding T, logically, must accelerate PC.
Well, it's logical, but not true. It was simply assumed. What was in fact observed is that sometimes adding T actually was beneficial, but sometimes not.
This observation, though, would also seem to contradict the idea that E2 necessarily promotes PC. After all, if there was no aromatase inhibition, then men given T would also have an increase in E2, so the men whose PC symptoms benefited from higher T must have not been harmed by the concordant rise in E2 levels. (Unless for some reason they didn't rise?)
If estradiol promotes PC, and if estradiol wasn't kept in check in all early attempts at high-T therapy, then it would seem that high-T therapy would NEVER work. But the literature does not indicate that at all. So how crucial is an AI?
I am also wondering about Dr. Bob's protocol: does it always include AI (Arimidex) dosing along with T therapy? I cannot recall in his lectures hearing him worry about high E2 levels or any need to measure or inhibit E2. Perhaps I am wrong and just not recalling, but here's my question: what was the basis (either theoretical or observed) for assuming high E2 was a problem, since high-dose estrogen monotherapy was a pretty successful PC treatment option for decades? (I assume oral DES does result in high serum E2.) And why are the PATCH trials of transdermal E2 not showing problems?
It is interesting to read Huggins, as he seems to suggest three possible interventions: removal of T (androgen deprivation), or high-dose estrogen OR high-dose T (two modes of hormonal interference). The third intervention dropped off the radar because of the faulty logic I mentioned above, and the second dropped off because of the high morbidity associated with oral DES.
I wonder if estrogen therapy will ever make a comeback, in the mode of transdermal E2. Seems to be getting trials in the UK (it's cheap!) but totally ignored in the US. I am trying to find an MO in New England, as opposed to Old England, who is willing to try it with me.
Heard of any MOs on the East Coast who use it, or high-T therapy, for PC?
I agree and I think that part of the issue is that PrC is heterogenous. Also, people respond to T differently - e.g. I aromatize a decent amount of it (as shown by my labs). So, if for no other reason, I like taking an AI to stop my bloating and gyno. I've tried 3. First two didn't work very well but the third one (Letrozole) worked so well I had to reduce the dose.
Dr. Bob doesn't seem to think an AI is needed. Dr. Friedman is convinced it is but he also seems to put a lot of stock into the heterogeneity of PrC.
Unfortunately I don't know of anyone on the east coast that do high T for PrC.
Dr. Bob will do teleconferences (that's what I do). But they aren't covered by insurance. $550 each quarter but I'm thinking it is worth it for now (covid might force me to change my mind if things get tighter financially). But I'm going to talk to them and see if I could do my labs locally once a quarter and do the teleconference once or twice a year.
When I did ADT I used estrogen to reduce my T (I was promptly told by 4 different doctors that E would not work - some of them even said that it wouldn't do a thing but one actually said it would lower my T but not enough - well, got it to undectable levels). Patch is cheap and effective and doesn't have all of the side effects of lupron. Note that I did zytiga at the same time but my T started going very low before I started zytiga.
Strange that many doctors themselves don't really seem to follow the literature or understand the science, so far as the feedback mechanism that causes a shutdown of T w/ exogenous E2. (My daughter is in med school and she agrees it is more about "learning the trade" than in being science-minded.)
Dr. Friedman seems to be on the right track, but I suspect his model oversimplifies how alpha and beta ER are under/over-expressed in different men under different conditions of disease, diet, meds, etc.
Nal, I agree that supra T is not TRT by any stretch. I notice a few times you have said the body doesn't recognise exogenous T. But synthetic T is identical to bio T. They are the same molecule. I get that there are possible isomers but synthetic T is usually made from cholesterol, which has the correct conformation to produce bio identical T. The body cannot distinguish the two, they are chemically identical, including isomeric conformation. My body certainly recognised supa T and produced alarming amounts of estradiol in response until the exogenous T cleared my system.
Glad you asked that, as I’ve been trying to interpret too. The post begins with saying ADT (as monotherapy) is not immunosuppressive, which to me means it does not suppress the immune system—which is good. It then says testosterone (normal-high levels) is immunosuppressive, which is not good. I’m particularly interested as my husband is supposed to start ADT this week; in 6 months will do brachytherapy followed by external radiation a month later-staying on ADT through it all & longer.
We need to be controlling inflammation. I have posted on this for PCa, but we need to double-up when ill with something that may turn out to be COVID-19. The immune response itself will add to inflammation. With a vigorous immune response & high inflammation we might suffer heart damage.
Normally, we want to face a virus with a healthy immune system. But with a heart issue, perhaps it's better for the immune response to be muted. Testosterone [T] is immunosuppressive and a high-normal T may be advantageous for some.
Here is one of many references to T & the immune system:
"we highlight the importance of testosterone in down-regulating the systemic immune response"
Hope this helps. The above is opinion, rather than medical advice.
-Patrick
Two years ago I abhorred drugs. But then I was diagnosed with PrC.
I didn't like the SOC prognosis and treatment future so I started tinkering.
Got my serum D up, inflammation down, WBC up, lipids down, carbon dioxide up, muscle mass up, fat down, estradiol down and changed a few other metrics (working on prolactin and DHT and BP). All thanks to drugs and supplements (all of it in my mind is similar at the core - chemical substances).
Strange how it took cancer for me to start changing my biology. I jokingly told my wife that I wish I would have gotten cancer 30 years ago.
Thanks for the book mention. I'm looking at it now on Amazon.
Some of the books I have on T:
New testosterone treatment by Friedman
The Definitive Testosterone Replacement Therapy Manual by Jay Campbell
Beating Prostate Cancer (Hormonal Therapy & Diet, 1) (Hormonal Therapy & Diet, 1) by Dr. Charles Snuffy Myers
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