A new meta-analysis of statin use and prostate cancer-specific mortality [PCSM] and all-cause mortality [ACM], below [1]. The analysis included 24 studies with 369,206 individuals.
It has been known for a century that solid tumors accumulate cholesterol. That may be reason enough to initiate statin use at diagnosis.
Castration therapy continues to be a "popular" PCa therapy. Early resistance continues to be common, even with add-on androgen-axis drugs. One form of resistance involves the generation of androgens from cholesterol - within the cancer cell. Statin use is insurance against that.
Some men say that their serum lipids are good & they do not need a statin. However, PCa cells may generate cholesterol itself, if serum levels do not meet their needs. Statins, which target liver production, can also prevent PCa cell generation. It seems that a lipophilic statin has the best chance of achieving that.
I have been on 40mg Simvastatin for 17 years. (I explained to my doctor that I wanted it for PCa, but you don't need a reason to get a statin script in the U.S.) I asked for Simvastatin by name, because of PCa sudies available back then. The FDA had recently banned the 80mg dose, although they did 'grandfather' those already on that dose. Studies have noted a dose-related benefit, regardless of brand, but I have been too lazy to look for the biggest equivalent dose among the 7(?) products.
Bottom line from the meta-analysis:
"... the use of statins is beneficial for ACM and PCSM, especially for postdiagnostic users. For patients who received either ADT or RP, statin use could decrease the PCSM. As for those who accepted either ADT or RT, statin use could decrease ACM. However, for patients accepting ADT, statin use may not always be beneficial for them."
For those puzzling over the " postdiagnostic users" comment, prediagnosis users include men in poor health, whereas postdiagnosis users man include many in good health (apart from the PCa, that is.)
Note, PCa, as with other cancers, and chronic diseases, is an inflammatory condition. The degree of inflammation affects mortality. There are a number of tests in the basic blood panel that relate to inflammation. I have relied on albumin as an indicator. <4.0 isn't good; my target is 4.5. (My albumin was 3.9 before prostatectomy. I used polyphenols, which are NF-kB inhibitors to get to 4.6..) Statins are anti-inflammatory. Unrelated to their effect on lipids. Anything that reduces subclinical inflammation will improve survival.
Very interesting study just a question read a study on a drug that stops prolactin old drug they have decided it has a lot to do with pca becoming castrate resistant Caroline I think the drug is called
"Concerned"? Yes, but I feel that inflammation is easily controled. My guess is that you are not taking hefty doses of apigenin, curcumin, fisetin, quercetin, or any others of the dozen or so that are commonly taken.
Avoid low doses, since we need pro-oxident doses IMO.
They all inhibit NF-kB, which is chronically activated in PCa. NF-kB is responsible for many cell survival proteins, including the COX/LOX family of enzymes that work on arachidonic acid to produce inflammatory agents.
Patrick, Your comment about low (anti-oxidant) vs high (pro-oxidant) dosage aligns with comments by mateobeach in a discussion about senolytics sometime back.
The first I remember hearing of the possible proactive influence of anti-oxidant on cancer was from none other than Jim Watson (of Watson and Crick DNA Nobel fame). That was around the time I had my RALP and the Open Biology paper linked below is the one that got all the attention at the time. It ran counter to everything I had read about anti-oxidants and it took me many years to start to fully question what had been the prevailing consensus. It is only with the recent rise in senolytics that I have become fully convinced of the dual dose-dependent role that anti-oxidants can play in preventing vs treating cancer. It also explains why IV vitamin C can be effective for cancer, while oral Vit C apparently never reaches pro-oxidant serum levels.
Oxidants, antioxidants and the current incurability of metastatic cancers - Open Biology, by Jim Watson, Published:01 January 2013
and a short 2017 article that provides some overview to Watson's perspective on anti-oxidants:
Dr. Watson's article in 'Open Biology': What are we to make of Dr. Watson's article in 'Open Biology', re: antioxidants may have caused more cancers than those cured?
A long time ago, my cholesterol was high, but my doctor at the time didn't like statins because "they could make you into a diabetic." So I increased fiber, cleaned up my diet and was fine.
Any thoughts to taking Red Yeast Rice to lower cholesterol and help in the good fight?
Patrick picked apart what I thought was "good" lipid panel back in 2019. His stated opinion is that "the triglyceride:HDL-C ratio is the most important part of a lipid panel". He considers 1:1 to be ideal and said he only get there when his T is normal. He further considers 2:1 OK, but getting into "insulin resistance territory". And with 3:1 being bad, and mine at the time at 2.36:1, he got my attention, which eventually led me to a RYR supplement.
This is what he wrote then about the dangers of high triglycerides for PCa patients:
* * *
Hi Cujoe,
My concern with the Tri:HDL ratio isn't cardiovascular - it's PCa-related. I have zero-tolerance towards insulin resistance because I feel that it is related to aggressive PCa. With insulin resistance, the body produces more as it tries to overcome the resistance. It's a growth promoter.
The irony is that the beta cells that produce insulin eventually burn out as a man becomes diabetic. A year later, the diabetic has reduced his risk of PCa. Not an ideal solution, but it points to the dangers of high insulin.
Best, -Patrick
* * *
In response to that message and the fact my HDL dropped out of the normal range, I eventually started using the RYR product recommended by another HU member who said it had tested as being the cap-for-cap equal to lovastatin. I started using that product , Cholestene, daily - taking 2 with my first meal and two at dinner. In just three months of use my lipids were brought to perfection. (See the attached graph.)
As always, your mileage may differ from mine, but I can't imagine a statin would have done any more to improve my lipid lab results.
There may be benefit in using RYR for synergy with other constituents. But beware:
"Some red yeast rice products contain a contaminant called citrinin, which is toxic and can damage the kidneys. In a 2021 analysis of 37 red yeast rice products, only one had citrinin levels below the maximum level currently set by the European Union."
I have used Atorvastatin 80 mg for some time. I agree that high cholesterol is fuel for PCa, I have interest in a different class of medicine and will be talking with my Cardiologist about getting put on Bempedoic Acid.
Omg, it's like someone is reading my mind or has a crystal ball into my current blood work.
Been fighting an escalating blood glucose since being on ADT. Was prediabetic during original PCa diagnosis in late 17'... Was able to control via diet alone 18-19’... But in 20' with the discovery of StgIV and the start of ADT it has been slowly increasing. 2018 (A1C) 5.9, 2020 9.0, 2021 7.6, 2022 7.9...
Using Metformin 2g per day, Creator 20mg but changed to 5mg due to Darolutamide being added. Also using prescription Omega III, Vascepa 2g per day (switched from Fenofibrate)...
Question is... Is there a Statin that does no have a contraindication with Darolutamide?
Also, I have the added complexity of developing kidney stones which had shown them to be Oxalate Calcium, so diet between glucose and Oxalates is a maddening minefield! Lmao... Welcome to a small window of my life!...
Again, question would be if there's a better known statin for use with Darolutamide. And maybe any suggestions as to who would be a good doctor (discipline) to see that would incorporate "ALL" of the above? Cancer doctors know cancer, but I've found not many delv into the unknown, or outside their expertise. This isn't a bad thing and is appreciated when they're honest. My regular GP definitely is honest too saying much of the above as a collective is outside his knowledge... So who then? And I'm not opposed to natural paths and supplements as well.
Lastly, thanks so much for the post/thread!!! It hit my radar screen bullseye dead center! (I'm scanning my home for eavesdropping devices right now) hahahahaha!
lipitor, zocor, livalo do not negatively interact with nubeqa. I'm taking livalo now. I might switch to lipitor in a month or two, depending on my next lipids and blood test results. Lipitor had the best results without nubeqa, crestor was second best, and zocor was very good as well. zocor was synergistic with nubeqa but I dont think they compared it against lipitor with nubeqa. I assume pipitor would be equal or possibly better than zocor. All of these are good though. Higher doses are better by a small %, if you can handle the high dose. Medium dosages are still very effective.
Thank you, I will look into these and see if the Doc is aware. In the interim, they reduced the Rosuvastatin to 5mg per day. Daro can cause it to be the equivalent of 5-10x dose... Crazy stuff, but I don't want to give up using the Statin either, so is good there are some absent contraindicated.
Now that I am about to start on darolutimide, I switched my statin away from Crestor, instead of lowering the dose. I want a more powerful dosage than 5mg of crestor, in order to counter the cancer.
Problem is which drug will have a higher efficacy towards the cancer ... And from my follow up to your post above, I've found (trials data) that all the statins have the same issue with Daro. It would be advisable to have blood work checked often as well if Daro+ Statins.
I can tell you it was only one day I took both full strength (20mg Rosuvastatin) and absolutely felt it! The next day I didn't touch the Statin and was on the phone with my doc's to sort it all out. The CYP3A4 interaction I suppose was responsible, funny thing is "EVERYONE" was aware I was using a Statin, but neither my GP or MO team made note of it...
Since the 5mg reduction, haven't had the episode again. Reducing the statin with the CYP3A4 effect isn't the same as getting less drug as the Statin or more of it stays in your system, no? Or am I missing something? Curious...
i think 40 should be enough. If you tolerate that, then you could try higher. Sone station can be split, if you take that kind of statin then you can try 50 or 60. See what your blood tests show on 40, before trying to go higher.
George he has gradually gone up over a year from 20 mg to 80mg. Blood work good. At 80 he was complaining of leg pain. We dropped it down to see if the statin was the problem. Not sure if that’s the problem. We will stay at 40 and gradually work our way up again. After reading all the posts and links, the statin and metformin doxy plays a big part in keeping everything at bay, as long as blood work remains normal. His last scans show nothing getting worse. We have scans in a few weeks. If you believe in the pathways, those drugs seem to block quite a few. I pull my own chart out and refer to it constantly!
It may be better to switch to the much more powerful PCSK9 inhibitor instead of a statin. Much more effective than any statin, even at highest doses. Two are available, sq injection every two weeks. Repatha is one, evolocumab.
Often used in addition to a statin but can be used without one.
And BTW, probably the best single test for lipoprotein cholesterol risk and adequacy of therapy is ApoB (Apolipoprotein B). Better than LDL-C and other rations. Triglycerides aside.
Good info Paul. I'm tracking wrt to the lipid info. What I am not aware of is the PCSK9 inhibitor. I will read your link. What doctor prescribes this inhibitor? Were any studies done, showing that the PCSK9 improved OS for advanced PCa patients?
Everything of importance to living a long and healthy life is not all about prostate cancer, even for those of us with Incurable APC. We need to look at the big picture about age related decline and risks of premature death from other causes as well. Risks of ASCVD as the #1 killer. These meds are underutilized game changers because they reduce risk twice as much as statins (on that order). Instead of ApoB under 60 you can get ApoB to 30s. That is big. Statins are good. PCSK9 inhibitors are better. Let’s expand the perspective and conversation.
very good support for the use of statins in men with APC. I also suspect that the anti-inflammatory effects may be playing a role in slowing PC progression as one of the main drivers of the “Hallmarks of Cancer”.
A couple of comments. Post diagnostic users were not necessarily healthier pre diagnostic. We know that greater attention to overall health and control of risk factors is often kicked into high gear at diagnosis.
There is a pervasive and unsupportable theory of that statins for reducing hepatic cholesterol synthesis will somehow deprive the cancer of cholesterol as “food” or precursors soft steroid hormones, etc. This cannot possibly happen. We have very much cholesterol in out bodies, in every cell and in every tissue. It is an essential component of all cell membranes. Nothing can function without it. It is everywhere and in abundance. Statins just reduce the excess of lipoprotein cholesterol that circulates, it does not go to zero.
That does not diminish nor negate the health benefits for ASCVD risk, the biggest killer of aging men and women in the end (by far). Nor the benefits of lipid control and inflammation reduction provided by statins and other therapies as others have mentioned. And PCSK9 inhibitors are probably much under utilized.
That said, this is a very valuable meta analysis. Paul
In addition, statins may also directly and indirectly upregulate tumor suppressor PTEN gene expression at the transcriptional level, which should be helpful. However, this mechanism also contributes to the statin-diabetes link.
Thanks for your always generous links to related research. Your number 5. link would seem to be an instance that confirms Siddhartha Mukherjee 's 2nd rule of Medicine (*):
"Normals" teach us rules; "outliers" teach us laws.
(*) from his book, The Laws of Medicine: Field Notes from an Uncertain Science (TED Books) Hardcover – October 13, 2015
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