#29

Thanks - I don’t think I want to go as far as sending blood off but will tell my doc about this and the option of 3 drugs. One thing I noticed looking through their tests though is that Interleukin 6 is an indicator of heart disease or inflammation. I went to Stanford for my chronic fatigue and they tested a bunch of those interleukins and 6 was in normal range. I looked back at the results during COVID because it was mentioned a lot in regards to that. Course, I was 60 then, not 71.

#30

Do any of you statin aficionados know if there is a real difference between the glycemic impact of long-term use of one statin vs another holding LDL-C lowering impact constant? E.g. any difference between 10mg of simvastatin and 20mg of pravastatin?

#31

It’s not from lowering LDL-c.

Atorvastatin > Rosuvastatin when it comes to diabetes risk.

Pitavastatin > Atorvastatin for increases in blood glucose.

#32

FWIW: I have been on statins of some kind since 1990 and never had any issues (that I know of…). I am almost 66 and take 10mg ezetimibe and 10mg rosuvastatin both in the evening. I also take fenofibrate 48mg in the morning. crestor IS a statin. ezetimibe is not a statin. I’m thinking of stopping the fenofibrate as my numbers are pretty good w/o taking it and it can cause issues in older people.

#33

(Post Deleted By Author)

#34

Just so it’s clear…

Atorvastatin is superior to rosuvastatin when it comes to diabetes risk and cataracts:

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#35

I say holding LDL-C lowering constant deliberately.

To the extent the glycemic impact is through HMG-CoA reductase inhibition it will be a class effect. I don’t need anybody to explain that rosuvastatin has a greater LDL-C reduction than other statins at the same dose, but that’s not the point.

I am interested in understanding if there are differences between the statins holding LDL-C impact (not dose) constant.

#36

Yes, like I told you, unless you believe the 0.1 mmol/L difference in HMGCR Inhibition is the cause.

#37

This is what ChatGPT said. It’s consistent with your two directional claims.

Statin Dose for ~25% LDL-C Reduction Impact on A1c Risk of New-Onset Diabetes
Pravastatin 20 mg Minimal to neutral impact Low risk, possibly neutral effect
Simvastatin 10 mg Slight increase in A1c (~0.1%) Moderate risk
Atorvastatin 10 mg Slight increase in A1c (~0.1%) Moderate to high risk
Rosuvastatin 5 mg Slight increase in A1c (~0.1-0.2%) Moderate to high risk
Fluvastatin 40 mg Minimal impact, possibly slight increase Low risk
Lovastatin 20 mg Minimal impact, possibly slight increase Low to moderate risk
Pitavastatin 1 mg Minimal to neutral impact Low risk
#38

The incidence of diabetes was 39% higher with rosuvastatin compared to atorvastatin at around the same level of HMGCR inhibition.

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#39

I am going to ask my doctor about pravastatin. I want to reduce my CVD risk for the long term, but I don’t need to nuke my apoB.

#40

Just to be clear I wrote about pitavastatin, not pravastatin.

I don’t worry that much about different statins except which one I tolerate the best, but based on the data lipitor seems safer than crestor.

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#41

There’s no generic for Livalo (pitavastatin) currently.

#42

Why do you prefer pravastatin over atorvastatin then, or even rosuvastatin?

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#43

Lower risk of negative impact on glucose regulation.

E.g.

Statins are a class of drugs widely prescribed as frontline therapy for lowering plasma LDL-cholesterol in cardiovascular risk prevention. Several clinical reports have recently suggested an increased risk of type 2 diabetes associated with chronic use of these drugs. The pathophysiology of this effect remains to be fully elucidated but impaired β-cell function constitutes a potential mechanism. The aim of this study was to explore the effect of a chronic treatment with lipophilic and hydrophilic statins on β-cell function, using human pancreatic islets and rat insulin-secreting INS-1 cells; we particularly focused on the role of mitochondria and oxidative stress. The present study demonstrates, for the first time, that atorvastatin (lipophilic) but not pravastatin (hydrophilic) affected insulin release and mitochondrial metabolism due to the suppression of antioxidant defense system and induction of ROS production in pancreatic β-cell models.

Atorvastatin but Not Pravastatin Impairs Mitochondrial Function in Human Pancreatic Islets and Rat β-Cells

For more discussion, focused on humans:

#44

Do any of you use a glucose monitor? Attia said they’re OTC just need a script, and that it’s kinda fun to track. Wondering if a good idea esp when on a statin. Livalo is the other one Attia usually starts his patients on, that or Crestor.

#45

I have worn a glucose monitor for two weeks at a time three times in the past year. I am pretty sure the simvastatin I was taking was pushing up my fasting glucose. That’s why I was interested in this issue, and why I specifically wanted to find the statin least likely to have this impact. I added ezetimibe so that I am asking for less LDL-C reduction from the statin.

#46

The more I learn thinking I might ask for the BrilloEZ Destrider takes and leave out the extra statin since my sugar is already 100. Have you thought of that?

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#47

A new Thomas Dayspring interview on managing lipids:

If you would like to hear my real-world description on pharmacological management of apoB - Here is another chat with @aaronhartmanMD of Richmond Functional Medicine that is only 17 minutes long.

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#48

It took me a while to come around to statins. I’m 69 and fit but have had a high cholesterol and Apo B - (a little higher than your numbers). So two things changed my mind. One was realizing that I was being hypocritical by being enthusiastic to take Rapa but suspicious and negative towards all other pharma. (I blame social media where so many “influencers” are completely wrong). The other factor that brought me around was spending time researching studies and listening to Doctors as to the specific mechanics of atherosclerosis. One of the biggest influences was Gregory Sloop MD a researcher who focuses on blood viscosity and hemodynamics. Wow, did he help me understand why you want to lower cholesterol as well as eat low fat.
Anyway, I started Ezetimide daily and Atorvastatin 4 times per week. I didn’t notice any changes in my strength or endurance and had no side effects. I tested about 2 months after starting these drugs and my total cholesterol was 134, LDL 52 and Apo B 54.
From my experience I wouldn’t worry about side effects. If you get muscle cramps or any of the listed bad effects you can talk to your doctor who now have lots of options to switch you to.
Finally, I also recommend focusing on your diet. If you read books by Dr. Esselstyn or others who use nutrition to cure cardiovascular disease you’ll read about studies of people around the world who have no heart disease in their populations. The commonality they have is that don’t eat like Americans.

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