One of our most esteemed members wrote "Don't take RYR [red yeast rice] and a statin at the same time. I use a statin a few weeks, stop a week, and then use RYR for a week, stop a week, repeat."
My cholesterol is minimal (last Total 146 Tri 42 HDL 93 LDL 45) so I would think a minimal dose of a statin and some RYR would be ok to combine at the same time??
Lol! Thanks for calling me an esteemed member!
Yeah, should be fine. But watch your liver enzymes (AST, ALT, ALP) and maybe GGT.
What kind of doses and what statin? Most RYR supplements don't have much active ingredient. For years the best has been HPF Cholestene.
Thanks, yes, I saw your earlier post on RYR and plan to switch to HPF next time.
I take 10 mg atorvastatin, just for PCa, cholesterol has always been ok.
Also, I inverted two of the numbers...'
Total 146 Tri 42 HDL 93 LDL 45
Should be
Total 146
Tri 42
LDL 93
HDL 45
I've always struggled with HDLs.
Calling you "esteemed" is much cheaper than paying for your medical advice.
First advice is free..... Trust me....
These numbers look pretty good to me. I live in the same podcast echo chambers as cujoe so not much to add, except I did a pretty deep dive into statins recently in order to lower my LDL and ApoB slightly (all fine-tuning at this point). I have been on low-dose (10mg) simvastatin, which my cardiologist friend says is "barely sniffing it", but am going to change to a slightly higher dose-equivalent of rosuvastatin (5mg) and test again a couple months. The main reason for switching is to see if I can indeed lower ApoB and increase HDL slightly.
Other considerations are lipophilic vs hydrophilic statins, metabolic pathways, any anecdotal data on apoptosis, PCa reduction, etc... I hesitate to switch statins, but also wonder if I'll notice any difference in terms of energy or mental clarity on the rosuvastatin in addition to the lipids. The rosuvastatin supposedly has fewer side effects or drug interactions too.
Stay tuned.
🥦
Lipophilic vs. Hydrophilic Statins
1. Mechanisms of Action
Statins (Lipophilic vs. Hydrophilic): All statins inhibit HMG-CoA reductase, thereby blocking the mevalonate pathway and reducing cholesterol synthesis. This reduction limits precursors for steroidogenesis, lowering intratumoral androgen production and disrupting lipid raft formation in cell membranes. Statins also decrease the prenylation of signaling proteins (e.g., Ras/Rho), which impairs cellular proliferation and induces apoptosis in prostate cancer cells. Moreover, they may reduce androgen receptor (AR) levels and signaling, thereby lowering tumor sensitivity to testosterone. Lipophilic statins (atorvastatin, simvastatin, lovastatin) are more cell-permeable, reaching prostate tissue and muscle more readily, whereas hydrophilic statins (rosuvastatin, pravastatin) act primarily in hepatocytes. Notably, lipophilic agents more potently compete with dehydroepiandrosterone sulfate (DHEA-S) for uptake via the SLCO2B1 transporter, thereby reducing adrenal androgen influx.
Red Yeast Rice (RYR): RYR is a fermented rice product containing monacolin K (chemically identical to lovastatin), sharing the same mechanism of HMG-CoA reductase inhibition. At typical supplement doses (~3–10 mg monacolin K/day), it modestly lowers LDL cholesterol. However, variability in monacolin content and the risk of citrinin contamination mean its anticancer effects are essentially those of a low-dose, less-regulated lovastatin.
Bipolar Androgen Therapy (BAT): Statins have no known role in the androgen-driven DNA break mechanisms of BAT; mechanistically it does not appear to synergize with BAT.
2. Stages It Might Be Applied To (nmHSPC, oHSPC, mHSPC, nmCRPC, oCRPC, mCRPC)
• nmHSPC: In localized prostate cancer managed with surgery or radiation, statin use has been associated with lower biochemical recurrence risk, particularly post-radiotherapy.
• oHSPC & mHSPC: In hormone-sensitive metastatic disease, retrospective evidence suggests statin users experience a prolonged response to androgen deprivation therapy (ADT) and improved overall survival, likely due to reduced androgen synthesis and growth signaling.
• nmCRPC: In non-metastatic castration-resistant disease, while trial data are lacking, the theoretical benefits of reduced androgen levels and anti-proliferative effects suggest a modest delay in progression.
• oCRPC & mCRPC: In advanced castration-resistant prostate cancer, observational studies indicate that concurrent statin use is associated with improved prostate cancer–specific and overall survival, possibly by sensitizing cancer cells to concurrent therapies.
3. Research & Studies
Recent observational studies and systematic reviews (from the past 5–10 years) consistently associate statin use with improved outcomes in prostate cancer patients. In mHSPC, a retrospective analysis showed statin users had a significantly longer time to castration resistance. In mCRPC, studies have reported a 53% reduction in risk of all-cause mortality among statin users. Preclinical studies further confirm that lipophilic statins induce apoptosis, reduce proliferation, and impede metastasis in prostate cancer models. RYR, although effective for cholesterol lowering, lacks direct clinical evidence in prostate cancer and is extrapolated from lovastatin data.
4. Overall Quality of Evidence
• Quality of Evidence: B – Moderate quality, largely based on retrospective and observational studies.
• Theoretical Rationale: A – Strong rationale supported by robust biochemical mechanisms and epidemiologic correlations.
• Preclinical Evidence: A for lipophilic statins; B for hydrophilic statins; D–C for RYR (limited clinical data, theoretical benefits).
5. Conclusion
Lipophilic statins (atorvastatin, simvastatin, lovastatin) and, to a lesser extent, hydrophilic statins (rosuvastatin, pravastatin) appear to confer ancillary benefits in prostate cancer management. Their ability to reduce cholesterol-driven androgen synthesis and interfere with growth signaling provides a strong theoretical basis for use alongside standard treatments, especially in hormone-sensitive and advanced disease. Red yeast rice, while offering similar mechanisms in principle, lacks robust evidence and should be considered primarily as a lipid-lowering supplement. Prospective randomized trials are needed to confirm these observational findings. Statins are not expected to interfere with BAT.
________________________________________
6. Common Side Effects
Muscle aches (myalgia), elevated liver enzymes, mild gastrointestinal upset, occasional sleep disturbances, and fatigue are the most common side effects. Lipophilic statins are more often associated with muscle complaints, whereas hydrophilic statins may have a lower incidence. Red yeast rice carries similar risks, with additional concerns regarding product variability and potential contamination.
7. DNA Damage & Double-Strand Breaks (DSBs)
Preclinical studies indicate statins can impair DNA repair mechanisms, acting as radiosensitizers by delaying repair of radiation-induced DSBs. This effect could theoretically enhance the efficacy of radiation and radioligand therapies, and possibly PARP inhibitors, although clinical data are limited. Statins do not cause significant DNA damage on their own. Regarding BAT, statins are not expected to interfere with its mechanism—mechanistically it does not appear to synergize with BAT.
This is from Gemini and pretty much aligns with what I've found. Gemini writes better than me though.
Fred (also a most esteemed member here),
FWIW, I use (exclusively) the RYR product, Cholestene. My initial use was based on a personal "review" of my then-recent lipid history by emeritus esteemed member, "Sir" Patrick O'Shea (who continues the be unfairly restricted from participation here), of what I had considered a fine lipid panel circa 2019. Patrick believes (as do many docs) that the triglyceride-to-HDL ratio (*) is much more important than is LDL-to-HDL - as it better reflects one's relationship to insulin resistance (and, thus, systemic inflammation). After my next lipid panel a year later came back with HDL below range, I started Cholestene at the recommended dose of 2 caps x twice a day - at or just before meals. The attached table shows the radical improvement I got after just 3 months of Cholestene supplementation.
BTW, I chose Cholestene as result of a post some many years back at "another forum" that said ConsumerLab had tested various RYR products, with Cholestene being the only one that matched a scripted statin, in that case it was lovastatin. My understanding from way back, is that RYR products came to market before statins - as the first statins were produced from RYR. Once the pharma products were FDA approved and chemically synthesized, the RYR products were restricted from advertising their statin equivalent content. In the ConsumerLab test of RYR supplements it indicated that many RYR products have little-to-no active statin agents. Thus, with supplement companies being unable to state whether they have any such ingredients in their labeling or their advertising, choosing a RYR for cholesterol control is a true random toss at the supplement dartboard. My personal experience with Cholestene has been impressive and consistently so. (See my dosage adjustment results and the attached table.)
However (and maybe due the ConsumerLab tests), the FDA has the following "Public Notification" about Cholestene, claiming it has "hidden ingredients" - which is, of course, its single unnamed active ingredient LOVASTATIN!!!!
Public Notification: Cholestene contains hidden drug ingredient
fda.gov/drugs/medication-he...
It is a similar situation to David Sinclair's touted longevity "supplement", NMN, which was banned once it began being used in clinical trials, and also for NAC which was banned for OTC sales several years back. (I used NAC immediately before and after my PSMA scan to help offset potential radiation damage as the radionucleotides made their way in and out of my body.) BTW, both NMN and NAC are now available again at Amazon and most online supplement companies, while Cholestene is not on Amazon and only available at a select few supplement companies.
neuroganhealth.com/blogs/ne...
npanational.org/news/npa-wi...
A bit like you, Fred, late last year I had a Labcorp walk-in Lipid Panel and saw that my triglycerides had dropped considerably, so I decided to cut my dosage in half; i.e., to 1 cap twice a day with meals. A more recent lab in January seemed to indicate that was maybe too much of a reduction, so I am now testing 3 caps per day, one with the first meal of the day and 2 with the last one. I'll maybe do another Lipid lab with my next Male Hormone Panel next month. That should determine if I can stick with 1+2 caps per day or should go back to 2 x 2. (BTW, LEF has just started their annual 25% off sale on all labs.)
For anyone who wants to truly understand lipids/cholesterol, Peter Attia has a recent single podcast that summarizes and updates the important information that was covered in the multiple podcast series done years back with Tom Dayspring, a world-renowned expert in clinical lipidology. Much of this podcast challenges the commonly accepted understanding of what to test and look for in improving one's lipid profile; i.e., how many people have been tested by their PCP for apoB. Dayspring is a wealth of knowledge and his podcast with the always informative Attia is well worth 2 1/2 hours of your time - with most of the last 1/2 hour on emerging knowledge about cholesterol synthesis in the brain and its relationship to brain function/health.
#334 - Cardiovascular disease, the number one killer: development, biomarkers, apoB, and more, Feb 3, 2025 The Peter Attia Drive Podcast
youtube.com/watch?v=5hiLY5o...
Finally, I'm not clear why you would want to use both a RYR supplement and a pharma statin when either one should be able to do the job. I originally decided to pay more to use both Cholestene over a scripted generic statin and berberine (+ milk thistle) over metformin. Now, I'd have to stop them and let my lipids and glucose rise, to get any doc to write a script for a pharma product. In both instances, I've gotten the results I wanted without any apparent side effects or negative interactions after 4 years on Cholestene and several years longer on berberine+.
I hope all remains well with you. Job #1 for all of us is Staying S&W, so keep it that way.
Ciao - cujoe
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(*) for Trig/HDL ratio, 2 is the target and 1 is perfection.
Radical improvement indeed! I just listened to that podcast a couple weeks ago.
Have you tested ApoB changes as result of Cholestene usage?
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Hey, My Northern Flyboy Friend,
Even though Attia has made much of its value even before this podcast, I have never tested for ApoB I meant to discuss it with my PCP back in Jan, but as he is also a sailor, we spent more time talking boat stuff than medical stuff. I did get my usual lipid panel, vit B-12 +D, and added a non-HS CRP for the 1st time ever this year . . . but completely forgot about asking about ApoB. (He might have hesitated anyway, as my current lipids would probably not suggest that I needed it.)
I'm doing some walk-in labs next month and will probably add it to the list - with LEF's 25% sale price being $21. (As I mentioned in the above reply, they are now having their once-a-year 25% off sale on all labs. I'll buy up what I expect to need for the rest of the year and ration them out over the next 9 months)
My current issue is getting my glucose down (80-90 range target). With an overnight fast, it consistently runs around 100 (tipping point for being pre-diabetic), so I'm soon going to get a finger-prick glucose meter and do some food-response testing to see what I might tweak with the diet. Unfortunately, each of the 3 drug- combo I'm using is known to affect blood sugar/glucose. So, I may have to take the good (T-boost) along with the not-so good (+ serum glucose)?
I'm headed out to the park for a run (upper-to-mid 70s F), so let's catch-up by phone sometime tonight? Give me a call anytime after ~ 7:30 PM, as I'll also hit the Y and do some grocery shopping on the way home. I'll say "hello" to the resident and transient bird population for you and the Hipster Bird Lady" on my run. I think of you two (fondly, of course) every time I'm there. Hope/Trust all remains well with you both.
Catch Ya' Later, Ciao - cujoe
BTW, when one of your docs balks at doing a CBC,CMP, or Lipid labs, tell him/her you can get all three done by Labcorp via LEF for a grand total of $35 US. (Sale price = $26.25). With the blood draw done in my case at a Labcorp/Walgreen's facility and then having to get transported to the nearest Labcorp testing center about 200 miles away, and some profit being distributed to all the parties involved, my guess would be that any medical facility with an in-house lab could do all three for less than 1/2 that cost (for staff time, disposable needles/vials, reagents, and equipment maintenance/amortization, etc.) Juz sayin'.
Copy that... and good to hear from you. I'm not tuning into HU as much as I used to so delayed in responding.
I think non-HDL-cholesterol is a good proxy for ApoB. With your excellent lipid profile I don't think ApoB is much of a concern. Just a curiosity.
I am one of the minority, unlucky ones, that has moderately high Lp(a), but otherwise lipids look good. Nevertheless, I might try to lower ApoB a little more since it's a variable I can control.
All good here. 🙏
I'll call tonight or this weekend.
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"My current issue is getting my glucose down (80-90 range target). With an overnight fast, it consistently runs around 100 (tipping point for being pre-diabetic)"
I was thinking about the glucose comment above. It's been on my mind because I know you are very healthy and conscientious eater and exercise regularly. Have you measured HbA1c? Considered a CGM to see what's spiking it and tweak accordingly?
I suppose if it's just the drugs, then you just have to take the good with the not so good as you said. Knowing you, you'll figure it out and have multiple graphs and a Power Point presentation ready in a few weeks 😀.
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Thanks for the suggestion. I have never had an A1c lab, but am delinquent in not having already gotten a glucose meter and done some food response testing. It has been on my "Get To Do"(*) list for a very long time, so it is a "get-to-do" for this week. I'm pretty sure I will find, like most people, that some unexpected foods, individually or in combination, have a tendency to spike my glucose. That should be enough to allow the dietary tweeks to hit my fasting target - even with any impacts from my current meds.
(*) I read somewhere last year that adding a "Get" to a "To-Do List" flips the physiological frame from a somewhat negative reference to a positive one; i.e., "Gee, I GET to do all these things vs I HAVE to do these things. Try it out and I think you will see for yourself that it does have positive power.
PS - enjoyed the catch-up call. Look for a follow-up email tonight. Stay S&W
Say it isn't so -- Patrick restricted here, on this particular arm of HU? I thought this was the un-moderated area, free of undue censorship or restrictions.
Yes, he has been so for well over a year now - with the outrageous circumstances for it unquestionably frivolous (and seemingly vindictive) - to say the very least!
Un-moderated? Well, not really the case when the risk of a potential loss of eyeballs elsewhere is more important than fairness and living up to the HU mission statement:
* * *
Empowering self-care
Imagine a world where everyone can share their experiences of healthcare, free from stigma or judgment. Where you can talk to people living with similar medical conditions, and gain support from caregivers and patient organizations - whilst also improving your health outcomes.
That's what HealthUnlocked from PPD, part of Thermo Fisher Scientific does. We provide the information, support and expert-curated resources to change lives. We're also a research tool for clinical development, helping pharmaceutical companies put the most important voices at the heart of research: people.
Interesting info, thanks. Why use both? No good reason, using a minimal amount of both seems like a good way of covering more possibilities than using a single agent.
BTW (& completely off-topic), being a ciga has been an excellent place to be over the last year+. Stay the course for a bit longer - or time ot jump ship?
No idea about the short term, but I am all in for the long term. (That I have a possible "long term" is thanks to Nal, Patrick, Learnall, and many others). Sinclair's expectation was an official revaluation at near the highest price (he wobbled between 90% and 97%).
A shame Sinclair is not around to see the recent breakout. I also note that I owe a debt to many "banned", "erased", "restricted", and current HU members for their help in keeping me "in the game of life". We all look to pay it forward whenever we get the chance. Enjoy spring when it finally gets to your part of the country.
BTW, I saw your old associate, L. Summers, make some very insightful "smartest-guy-in-the-room comments" about the long-term effects of an escalating tariff war Black Swans everywhere you look these days..
Saw his comments, totally agree with them (not with a lot of his stuff, but certainly agree with the paper that cost him his Harvard presidency). Before his ascendance I had a couple of X exchanges with Miran, who now, as chairman of the economic advisors, is navigating that path. He seems to be a knowledgeable trader of financial instruments for what that is worth.
How do we pay it forward if we are not smart enough to keep up with the stars here (I am serious, I will never reach the level of Patrick, Russ, etc.)?
To be clear, Dr. Summers was way above me, not as "associate", I was a foot soldier in a job I had taken on the international side of Treasury after a buyout from my corporate job.
So, you must have just called him "Doc" when to two of you were chewing the international financial fat over a couple of Guinness brews down at the nearest pub? 🙊 🙉 😎 ☮
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