New study from Canada. Laurence Klotz was a co-author.
Yet another meta-analysis, but appearing in JAMA might help get the message out.
"Twenty-five cohorts of 119,878 men (65,488 statin users [55%]) with more than 74,416 deaths were included.
"Concurrent statin use was associated with a 27% reduction in the risk of overall mortality ... and a 35% reduction in the risk of PCSM .., with substantial heterogeneity in both estimates.
"Subgroup analyses identified a PCSM advantage associated with statins for men receiving ARATs compared with ADT alone (HR, 0.40 ... vs 0.68 ...)..."
Thanks for sharing - interesting. This is something I'll review with my MD.
I had been holding off on statins while going through ADT+ (nubeqa), chemo, and SBRT for early/low volume BCR.
I also had a moderate risk coronary calcium score (19), but avoided adding statins given the QoL impacts from everything else. I tried Lipitor for a few weeks and it made me even more fatigued.
Patrick, greetings, Great to see you posting at FPC.
I wonder if you could explain if ARAT’s are just the medications usually referred to as second line treatments - the androgen receptor inhibitors - or something different?
Some years ago, when patients who had become resistant to enzatutamide or abiraterone discovered that they had also become resistant to the other drug, experts were saying "Of course! They do the same thing!" I found that puzzling. Enza is an AR antagonist, whereas Abi is a hormone suppressor.
But the target of both drugs is ultimately the androgen receptor [AR], or better, "the AR axis". Before there was Abi & Enza, going back years, we had ADT & all the early "lutamides", so there's nothing new here.
And that's the flaw. Doesn't matter how these & newer AR axis drugs are combined, it's still monotherapy. Works for a while. Needs to be couple with something unrelated to the AR, IMO.
Thank you Patrick. I was a bit confused by the 'axis' inclusion. I understand now.
Maybe your comment 'works for a while' is why our MO told my husband last month he expected the Abi to work basically for total of two years.
Guess it might go on the individual profile of each person. I know every one is different. You read on HU about people being on it for years and years with no increased PSA so suppose given that most would be on Lupron (or similar) and Abi... it's those unknown/other factors that make it work for some and not so for others.
In 2004 I was 56 and not happy with the options of the time. Lupron was said to fail between 18-24 months. Then there would be Taxotere for a few months. I might not even see 60.
That's when I became very interested in testosterone [T]. I have been using T to reset the ADT clock, every three months. In a month, I will be 75. A milestone I never expected.
One of the problems with posts by men who have been on Lupron for decades, say, is that they don't seem to have done anything special to beat the odds. Impossible to emulate with any expectation of doing better than the 18-24 months that the vast majority faced. And those men aren't around to tell their side of things.
What Abi has done is to add a year, say, to that 18-24 months, before CRPC sets in.
So, if I were newly diagnosed at age 56, I would still consider using T as a reset.
Denmeade is using BAT on men with CRPC. Good for him - those men have few options. But my plan has always been to avoid CRPC.
I should add that I never looked for a "cure" - I settled for second best: "management".
Yes, I inject testosterone cypionate into thigh muscle.
I am using DES (Diethylstilbestrol) for ADT. It is an oral estrogen, so I can stop using it for 7-10 days. For non-oral ADT, you just stay on it. The T will override it.
I think that is enough for my purpose. It will raise T above 1,000 ng/dL after a few days.
When I feel like giving the Denmeade dose a try, I self-inject the same dose into the other thigh. Denmeade likes to get to 2,000 ng/dL because that may induce double-strand DNA breaks in PCa cells (but not normal cells.)
So far as I can tell, he has never had a trial where both doses were used. I would like to see proof that the dose makes a difference.
Also, I have never seen reference to hematocrit testing. T replacement restores red blood cells & reverses anemia. But in a few men, the red blood cell count can get too high. I don't know if the 2nd dose increases the risk.
pjoshea13 wrote -- " ... Also, I have never seen reference to hematocrit testing. T replacement restores red blood cells & reverses anemia. But in a few men, the red blood cell count can get too high ... "
Just a how different we are --
My injection of 1ml Cypionate 200mg/ml raises my T to at least 1,600ng/dL following injection with a decline to 450/650 before next injection in 2 weeks and in the years since beginning (2016) I've remained at anemic levels with low hematocrit for the majority of time.
Patrick - Welcome back, Old Man and an early welcome to the 75-and-older community. You've had a near record run of beating SOC and advancing the PCa-knowledgebase at the same time. I'm about 13 years out from initial diagnosis and 9 years from RALP+IMRT.
I'm currently using bical "intermittently" in a self-treat program after doing a 2-month repeat of the initial 3-mo lupron treat that got me 4 1/2 years of <0.1 vacation. (There is a puzzling story to the 2021 BRC #2, but that is probably irrelevant to my current situation.) I remain a "good responder" to ADT and am able to get a sub 0.1 PSA response after several months of either lupron or bical, but since BCR#2, I have not been able to get one that is durable.
I tested last Thursday with an all-time high T of 773 due to a month of bical 50 mg. That is up from an average of 450 (morning labs) during the 4+ year vacation and 617 after the recent 2 mos of lupron.
My E2 is also sub 20 even with the high T, which seems a bit odd to me.
I know bical can boost T by up to 50%, but my question is whether this would in any measure provide a similar benefit as TRT?
Appreciate any insights you can provide. Ciao - Capt'n cujoe
PS I found that the people who know the most about the interplay of human hormones are the transgender docs. This site is a good one for info:
I learned much of what I know about hormones from bodybuilding sites. I'm the least likely guy to be a member. Those guys are results-oriented. Nalakrats would fit in. The guys running them better know their stuff. Thanks for the link.
There are two types of TRT situations. The first is where a doctor grudgingly aims to get T above 350 ng/dL - but not by much. Some still use 300 ng/dL as the cutoff for hypogonadism. 350-1,000 is a crazy-big range for "normal" & I would want to be in the upper third of that range, as in 773 ng/dL. On the other hand 450 ng/dL is pretty good compared to many men at PCa diagnosis.
(The other type of TRT is where a middle-aged guy wants to be at age 21 levels again. So he bypasses his doctor & goes online.)
With a T value of 450, I would be looking at the E2:T ratio. For instance, 35:450 would worry me - but 20:450 not at all.
You say E2 is sub 20 - hopefully not too sub. Below 12 pg/mL there might be bone loss.
Do you take an aromatase inhibitor?
When PCa cells lose the ERbeta estrogen receptor & gain ERalpha, the cells can also start to make aromatase. Blood tests don't detect what happens in the privacy of a cancer cell when T levels are normal.
Thanks for the reply. No AR inhibitor ever, just lupron & bical (with a short 30 day test with bical + dutasteride a year and a half back.) Two seeming anomalies I am trying to decipher are:
1. Low E2 in presence of normal to high T. (I guess I'll have less worry about manboobs and more about bone mass?!?) E2 has risen closer to 20 with latest Labcorp lab.
2. Low free T to Total T ~ 1.1+% vs desired/expected 2%. (percentage has been near same for last two labs - and was less than 1% for the first one? Any solid suggestions for increasing free ratio? (It is slowly creeping up with increasing T.)
I would guess that low free-T is due to elevated SHBG. I associate high SHBG with high estrogen (which you don't have). Stinging nettle root supplements can bind to SHBG, leaving less to bind to T.
(SHBG falls as T rises. Always seemed odd to me - as T rises, free-T will rise too, but with SHBG falling, free-T gets an extra boost.)
Thanks Patrick. I'll give the Stinging Nettle Root a try. I've also never tested for SHBG, so I'll see if I can get my PCP to do that for me at my annual visit later this month.
As for being an interesting case, it would be nice if I could find an MO who also saw it that way. 😠 Seems non-SOC = thorn in their sides.
Patrick - I started this about 5 days ago, but just now have gotten it finished.
Don't know if you are familiar with Dr. Peter Attia, MD, (The Drive Podcast) or Dr. Andrew Huberman (Huberman Lab), but I re-listened to this podcast last night (4 days ago) and it confirmed your comments on my T vs Free T vs E2 disparate lab results. It also goes into great detail about the relationships between them. Attia is unique, in that he is an MD who is focused on fitness and longevity (healthspan+lifespan) and runs a clinical practice that is constantly searching for better ways to improve each. So, you might say he is practicing what he preaches and, as a result, definitely has substantial "skin in the game".
Both he and Andrew Huberman are experts in their respective fields and each generously shares their knowledge and experience with the public through their websites, podcasts. They both are also frequent guest with the most-popular hosts of health-related podcasts on the web.
Peter's podcasts are all infused with the hands-on experience he continues to gain in his clinical practice. This podcast is somewhat wide-ranging, but contains lots of info we can use to improve our health and fitness. The relevant male hormone discussion begins around the 1:25:00 timeline. There is even mention of your SHBG-binding Stinging Nettle somewhere along the way. The full content timestamp listing is at the bottom of the linked page.
Patrick, you've obviously done extremely well with the choices you've made in regards to treatments. The more I read the various posts it seems that you really need to be well researched as you are and then make your own choices.
And you're right about Lupron...it held good for bit under 2 years before my husband became castrate resistant...he had been advised to expect about 17 months so that was pretty accurate. Your comment about 'expectation' is a bit of a reminder for me that they are mostly outliers - those who have excellent responses.
I'm familiar with the use of testosterone and the alternative/alternate therapies but it would seem, at least here in our country, even in the major cities, it's not easy to access treatments that aren't considered SOC. I can't imagine my husband's MO supporting testosterone injections. I couldn't even talk him into a change from Enza to Dauralutiminde (off label) and I didn't think that was such a radical suggestion.
It's sort of like a minefield...because you might know that some medications (or a break) would possibly present a better choice but you are locked into a system and it just become easier to go with it.
I don't think 'cure' either but I do encourage my husband to try to develop a mindset of prostate cancer as a chronic condition in the hope that it makes things a bit easier and helps develop a mentality of just ongoing management.
Thank you for taking the time to explore this issue a bit with me. Most appreciated. Marnie.
Marnie - see my latest comment to Patrick re: non-SOC patients. Tell Mr, Ron that that garden of his needs some weeding and watering - as summer is coming to the Land Down Under. (Where women glow and men plunder . . .)
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The Science is Coming as Fish Says
My new Oncologist needs learning curve help!
Androgen Receptor Activity (ARA) for BAT
